Hytro BFR seeks investors for fitness industry expansion – Endurance.Biz

Hytro BFR (blood flow restriction), has announced a follow-on investment round to continue its growth in the strength and recovery market through its patented TechWear garments, which are claimed to increase muscle and speed up recovery.
The company points to a muscle growth and recovery market set to be worth US$5 billion by 2027.
After a successful funding round earlier in the year, Hytro is looking to secure an additional £1 million in early 2022. Hytros plan to use the capital to develop new products and expand the team after a fast growth period.
The brand claims to be ‘scientifically proven to increase muscle size by 31% and accelerate recovery time by 33%.’
‘Hytro’s BFR straps trap blood in the muscles causing them to swell and become stressed. This can increase muscle fibre activation and up-regulates muscle building hormones.’
Since launching, Hytro has been used by coaches, practitioners and athletes in elite sports including players from rugby league teams, Leeds Rhinos and St Helens.
The company states… ‘Mainstream media publications and national newspapers are tipping this as a rapidly growing trend amongst fitness enthusiasts, featuring Hytro as a pioneering brand delivering products to the consumer market.’
Raj Thiruchelvarajah, CEO and Co-Founder of Hytro, said “BFR training has been around for many years but has yet to go mainstream. The benefits are backed by a substantial body of research but the cumbersome products available have limited its use.
“At Hytro, we’re enabling everyone from elite athletes to newcomers to build muscle and recover faster with our safe and easy to use patented BFR TechWear. With sales and interest from some of the UK’s biggest professional sports teams, organisations and Olympians, we’re looking forward to continuing our journey to take BFR to the forefront of training.”


Wireless 3D Printed Wearable Sensor to Track Health and Body Function – AZoSensors

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We decided to develop this new class of devices mostly because of the gap in the capabilities of current wearable devices. Form factors have not changed for a long time and shortcomings, including the constant need for device interaction such as charging and lack in sensor fidelity often induced by bulky device construction, restrict the devices’ capabilities significantly.
We started this project to overcome these limitations to enable the seamless collection of biosignals and provide a platform for new sensors that are enabled by intimate integration with the body.
Wireless 3D Printed Wearable Sensor to Track Health and Body Function.
Image Credit: University of Arizona
Biosymbiotic devices are soft electronics that are directly tailored to an individual to provide the best bio integration possible.
We solve the challenge by using 3D scans of the wearer to build a device that is unique to the individual. We have developed a technique to 3D print them, which has the benefit of being able to create unique devices and we can tailor sensor location to enable the best possible signal fidelity.
Our goal was also to create a system that is almost imperceptible to the subject wearing it, this is why we needed to eliminate bulky batteries. We achieved this by using a technique called power casting – a technique that recharges devices or even completely powers them in the proximity of this infrastructure. This means that users never have to recharge. In fact, as shown in our publication, devices stay topped up for weeks at a time.
The key benefits of the system are derived from the personalized structure that can intimately conform to the wearer. This enables sensor placement in the most relevant locations to extract high fidelity biosignals, opening up avenues to capture more information than with conventional designs.
For example, we can integrate stretchable strain sensors that allow for the measurement of muscle activation by sensing the circumferential change, which is currently not possible with wearable devices.
We can also integrate low thermal mass temperature sensors which enable the measurement of milli Celsius fluctuations that are induced by exercise. This is not possible with large devices such as smartwatches because they have too much thermal mass.
Another key benefit is the wireless power transfer that enables 24/7 operation. This results in the ability to provide uninterrupted data streams where typical solutions have to be taken off to recharge. The combination of the stretchable mechanics and the continuous operation also combats user fatigue which results in better device acceptance.
I think the reason why this was not attempted before is that some of the technologies were not available. Far field power casting that is now commercially available and is a fairly new development and the ability to 3D print elastomeric materials in an accessible way is also a recent development.The same applies for strategies for stretchable electronic circuits.
Our devices are a culmination of these novel techniques.
I have outlined some of the limitations in terms of sensors in my previous examples on temperature sensing where thermal mass of current devices is prohibitive, however one fundamental limitation for devices that are attached to the body using adhesives is the epidermal turnover of the skin, meaning the renewal of the skin. This turnover results in the renewal of the top layer of the skin every 5-7 days which poses a finite lifetime for adhesive based devices.
The epidermal turnover of the skin, meaning the renewal of the skin.Epidermal turnover of the skin. This turnover results in the renewal of the top layer of the skin every 5-7 days. Image Credit: Shutterstock.com/ tofuneko
The limitations of wearable devices such as smartwatches are typically the high mass which causes motion artefacts and limits the electrical contact to the skin, resulting in lower fidelity.
This is very beneficial for some sensor types, for example, if you would like to get something close to core body temperature we can make devices that place temperature sensors in the auxilia region (armpit) which provide a much more accurate reading than estimating this with a wristband based device.
We can also place new sensor types, such as our circumferential strain sensors, onto the area of the muscle with most deformation during exercise which provides an intimate insight into exercise intensity.
For biosymbiotic devices, the sensors have good contact with the skin and high fidelity bio data is able to be attained, even during extreme events. This advantage is immediately visible when compared to a classic wearable device that features a battery and strap attachment that is quite heavy.
During a jump, the mass of the device induces oscillations in the readouts that are not present on the actual limb. For our devices, that only weigh milligrams, this motion artefact is not present, highlighting a fundamental advantage. This will also be relevant for optical sensing techniques such as PPG and SPO2 measurements.
The application of biosymbiotic devices can range anywhere from diagnostic devices that allow for at-home detection and management of disease to human performance-related applications that characterize training and recovery. Devices may also be used to monitor the environment around the wearer and provide feedback.
As the devices are personalized, individualized sensor configurations may also be possible to cover specific scenarios, for example, for comorbidities.
The integration of many new technologies always poses challenges, especially when creating devices that are very different from the current state of the art. Luckily, I have a team of very talented graduate and undergraduate students that are dedicated to pushing the envelope and are very motivated to find solutions to the technological challenges we encountered throughout our research and for translation to products that are highly scalable.
I think we will see a lot more connected sensing solutions that make use of multimodal sensor systems that harness these data streams using artificially intelligent algorithms that will support the therapeutic and diagnostic decisions of clinicians.
Devices will also be used much more extensively for personalized health, meaning personalized training for athletes, personalized recommendations for diet and lifestyle and sensing our surroundings to optimize performance. This may also help with public health.
We are currently expanding the capabilities for biosymbiotic devices and exploring new sensing possibilities that are enabled by the platform. We are also performing clinical trials with devices to benchmark their performance against the gold standard to evaluate their use in automated at-home diagnostics.
Readers can find out more information on this work in our recently published paper which is open access. More information on the team is also available on our research group's homepage.
Dr. Philipp GutrufDr. Philipp Gutruf is an Assistant Professor in the Biomedical Engineering Department and Craig M. Berge Faculty Fellow at the University of Arizona. He received his postdoctoral training in the John A Rogers Research Group at Northwestern University and received his PhD in 2016 at RMIT University (Australia).
His research group focuses on creating devices that intimately integrate with biological systems by combining innovations in soft materials, photonics and electronics to create systems with a broad impact on health diagnostics, therapeutics and exploratory neuroscience. In the last 5 years he has authored over 50 peer-reviewed journal articles, received 5 patents and his work has been highlighted on 8 journal covers. More recently his group's work is featured in journals such as Nature Communications, Science Advances, PNAS and Nature Biomedical engineering.
Disclaimer: The views expressed here are those of the interviewee and do not necessarily represent the views of AZoM.com Limited (T/A) AZoNetwork, the owner and operator of this website. This disclaimer forms part of the Terms and Conditions of use of this website.
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Bethan has just graduated from the University of Liverpool with a First Class Honors in English Literature and Chinese Studies. Throughout her studies, Bethan worked as a Chinese Translator and Proofreader. Having spent five years living in China, Bethan has a profound interest in photography, travel and learning about different cultures. She also enjoys taking her dog on adventures around the Peak District. Bethan aims to travel more of the world, taking her camera with her.
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Dr. Philipp Gutruf
AZoSensors speaks with Dr. Philipp Gutruf from the University of Arizona. In their research, Dr. Gutruf and his team focus on creating devices that intimately integrate with biological systems by combining innovations in soft materials, photonics and electronics to create systems that have a great i
Dr. Tammy Chung
AZoSensors speaks with Dr. Tammy Chung from the Rutgers Institute for Health, Health Care Policy and Aging Research. In their preliminary study, Dr. Tammy and her team of researchers evaluated the use of mobile technology for substance use assessment and intervention.
Dr. Nanshu Lu
A new path has been set for pressure sensors with a flexible hybrid sensor breakthrough. AZoSensors speaks with Dr. Nanshu Lu to learn more.
Optris’ PI 05M is an infrared camera capable of measuring temperatures up to 2450 degrees. It is the perfect instrument for temperature measurement of molten metals.
For precise thickness measurements of plates, strip materials, and sheets up to 25 mm, use thicknessGAUGE Sensor Systems from Micro-Epsilon.
Discover the 4EM-5 with a photovoltaic four-element linear detector.
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Dyne Therapeutics Presents New In Vivo Data for its Myotonic Dystrophy Type 1 Candidate (DYNE-101) Demonstrating Robust Splicing Correction During World Muscle Society 2021 Virtual Congress – GlobeNewswire

| Source: Dyne Therapeutics, Inc. Dyne Therapeutics, Inc.
Waltham, Massachusetts, UNITED STATES
– New In Vivo Data Also Show Sustained Knockdown of Toxic Human Nuclear DMPK RNA and Foci Reduction –

– DM1 Program is One of Three IND Submissions Planned Between the Fourth Quarter of 2021 and the Fourth Quarter of 2022 –
WALTHAM, Mass., Sept. 20, 2021 (GLOBE NEWSWIRE) — Dyne Therapeutics, Inc. (Nasdaq: DYN), a muscle disease company focused on advancing innovative life-transforming therapeutics for people living with genetically driven diseases, is presenting new in vivo data during the World Muscle Society (WMS) 2021 Virtual Congress demonstrating the ability of its myotonic dystrophy type 1 (DM1) candidate, DYNE-101, to target the nucleus and achieve knockdown of toxic DMPK RNA, foci reduction and correction of splicing in muscle tissues in the hTfR1/DMSXL mouse model.
“DM1 is a spliceopathy, and in a novel hTfR1/DMSXL model, DYNE-101 demonstrated robust correction of splicing in the heart and skeletal muscles, as well as knockdown of toxic human nuclear DMPK RNA at a magnitude that has the potential to be disease-modifying. In addition, the subcellular fractionation data we generated reinforce that DM1 is a nuclear RNA-driven disease and that DYNE-101 effectively acts in the nucleus. We are also pleased that DYNE-101 was well tolerated in a non-human primate dose-range finding study,” said Oxana Beskrovnaya, Ph.D., Dyne’s chief scientific officer. “These findings further validate the FORCE™ platform as we drive our three programs toward the clinic, and we also look forward to presenting new in vivo data for our Duchenne program at the Muscle Study Group Annual Scientific Meeting in October.”
DM1 is a rare, progressive, genetic disease caused by an abnormal expansion in the number of CTG triplet repeats in a region of the DMPK gene that causes toxic RNA to cluster in the nucleus, forming foci and altering the splicing of multiple proteins essential for normal cellular function. As a result of this altered splicing, people living with DM1 typically experience progressive weakness of skeletal, cardiac and smooth muscles. There are no approved disease-modifying therapies for DM1. DYNE-101 consists of an antigen-binding fragment antibody (Fab) conjugated to an antisense oligonucleotide (ASO) to enable targeted muscle tissue delivery with the goal of reducing toxic DMPK RNA in the nucleus, releasing splicing proteins, allowing normal mRNA processing and translation of normal proteins, and potentially stopping or reversing the disease.
The new data being presented during the World Muscle Society Congress were generated using an innovative hTfR1/DMSXL mouse model developed by Dyne that expresses the human transferrin 1 receptor (TfR1) and carries a human DMPK gene with more than 1,000 CTG repeats that represents a severe DM1 phenotype. In hTfR1/DMSXL hemizygous mice, the data demonstrated that human mutant DMPK RNA was trapped in the nucleus of muscle and that DYNE-101 acted within the nucleus to degrade toxic human DMPK RNA. In hTfR1/DMSXL homozygous mice, DYNE-101 delivered sustained reductions in toxic human DMPK RNA (49 percent) and foci area (49 percent) in heart tissue leading to splicing correction at 4 weeks. Similar results were observed in skeletal muscle, with DYNE-101 demonstrating toxic human DMPK RNA knockdown of 40 percent in the diaphragm, 49 percent in the tibialis anterior, and 44 percent in the gastrocnemius, along with correction of splicing in each muscle at 4 weeks.
While not a disease model for DM1, DYNE-101 was also evaluated in non-human primates where it was found to be well tolerated in a non-GLP toxicology dose-range finding study. No adverse findings or clinical signs of toxicity were seen after repeat ascending doses of DYNE-101, and no effects on body weight, kidney or liver function were observed.
The poster (EP.233) entitled, “The FORCE™ Platform Achieves Durable Knockdown of Toxic Human Nuclear DMPK RNA and Correction of Splicing in the hTfR1/DMSXL Mouse Model” is available in the Scientific Publications & Presentations section of Dyne’s website.
DMD Program Presentation During Muscle Study Group Annual Scientific Meeting
Additionally, new in vivo data for Dyne’s Duchenne muscular dystrophy (DMD) program will be featured during the Muscle Study Group Annual Scientific Meeting, which will take place virtually October 1-3, 2021. The abstract entitled, “FORCE™ platform delivers exon skipping PMO, leads to durable increases in dystrophin protein in mdx mice and is well tolerated in NHPs,” has been published in the RRNMF Neuromuscular Journal. Dyne will deliver a presentation on October 1, 2021 and plans to issue a press release summarizing the data.
About Myotonic Dystrophy Type 1 (DM1)
DM1 is a rare, progressive, genetic disease that affects skeletal, cardiac and smooth muscles. It is a monogenic, autosomal dominant disease caused by an abnormal expansion in a region of the DMPK gene. The expansion in the number of CTG triplet repeats causes toxic RNA to cluster in the nucleus, forming nuclear foci and altering the splicing of multiple proteins essential for normal cellular function. This altered splicing results in a wide range of symptoms. People living with DM1 typically experience progressive weakness of major muscle groups, which can affect mobility, breathing, heart function, speech, digestion and vision as well as cognition. DM1 is estimated to affect more than 40,000 people in the United States and over 74,000 people in Europe, but there are currently no approved disease-modifying therapies.
About the FORCE™ Platform
The proprietary FORCE™ platform drives Dyne’s efforts to develop targeted, modern oligonucleotide therapeutics with the potential to be life-transforming for patients with serious muscle diseases. Dyne designed the FORCE platform using its deep knowledge of muscle biology and oligonucleotide therapeutics to overcome the current limitations in delivery to muscle tissue with the goal of stopping or reversing disease progression. The FORCE platform leverages the importance of transferrin 1 receptor, TfR1, in muscle biology as the foundation for its novel approach. TfR1, which is highly expressed on the surface of muscle cells, is required for iron transport into muscle cells. Dyne links therapeutic payloads to its TfR1-binding fragment antibody (Fab) to develop targeted therapeutics for muscle diseases.

About Dyne Therapeutics
Dyne Therapeutics is building a leading muscle disease company dedicated to advancing innovative life-transforming therapeutics for people living with genetically driven diseases. With its proprietary FORCE™ platform, Dyne is developing modern oligonucleotide therapeutics that are designed to overcome limitations in delivery to muscle tissue seen with other approaches. Dyne’s broad portfolio of therapeutic candidates for serious muscle diseases includes programs for myotonic dystrophy type 1 (DM1), Duchenne muscular dystrophy (DMD) and facioscapulohumeral muscular dystrophy (FSHD). For more information, please visit https://www.dyne-tx.com/, and follow us on TwitterLinkedIn and Facebook.
Forward-Looking Statements
This press release contains forward-looking statements that involve substantial risks and uncertainties. All statements, other than statements of historical facts, contained in this press release, including statements regarding Dyne’s strategy, future operations, prospects and plans, constitute forward-looking statements within the meaning of The Private Securities Litigation Reform Act of 1995. The words “anticipate,” “believe,” “continue,” “could,” “estimate,” “expect,” “intend,” “may,” “might,” “objective,” “ongoing,” “plan,” “predict,” “project,” “potential,” “should,” or “would,” or the negative of these terms, or other comparable terminology are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. Dyne may not actually achieve the plans, intentions or expectations disclosed in these forward-looking statements, and you should not place undue reliance on these forward-looking statements. Actual results or events could differ materially from the plans, intentions and expectations disclosed in these forward-looking statements as a result of various important factors, including: uncertainties inherent in the development of product candidates, including the conduct of research activities and the initiation and completion of preclinical studies and clinical trials; uncertainties as to the availability and timing of results from preclinical studies; the timing of and Dyne’s ability to submit and obtain regulatory clearance for investigational new drug applications; whether results from preclinical studies will be predictive of the results of later preclinical studies and clinical trials; whether Dyne’s cash resources will be sufficient to fund the Company’s foreseeable and unforeseeable operating expenses and capital expenditure requirements; uncertainties associated with the impact of the COVID-19 pandemic on Dyne’s business and operations; as well as the risks and uncertainties identified in Dyne’s filings with the Securities and Exchange Commission (SEC), including the Company’s most recent Form 10-Q and in subsequent filings Dyne may make with the SEC. In addition, the forward-looking statements included in this press release represent Dyne’s views as of the date of this press release. Dyne anticipates that subsequent events and developments will cause its views to change. However, while Dyne may elect to update these forward-looking statements at some point in the future, it specifically disclaims any obligation to do so. These forward-looking statements should not be relied upon as representing Dyne’s views as of any date subsequent to the date of this press release.
Dyne Therapeutics
Amy Reilly
[email protected]


Skeletal Muscle Is an Early Site of Zika Virus Replication and Injury, Which Impairs Myogenesis | Journal of Virology – Journal of Virology

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What Role does Endothelial Infection Play in SARS-CoV-2 Infection? – News-Medical.net

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The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can cause inflammatory lung disease, including clot formation and hyper-permeability of the lung vessels, resulting in edema and bleeding into the lung. Inflammation also affects other organs, mediated by the cytokine storm.
This inflammation is characterized by endothelial cell dysfunction in multiple organs. The cause of this endothelialopathy is unknown. It could be due to the direct infection of endothelial cells or an indirect effect of the cytokines.
SARS-CoV-2 Virus
Image Credit: Kateryna Kon/Shutterstock.com
Unlike earlier coronaviruses pathogenic to humans, SARS-CoV-2 has a spike protein that is linked to host recognition and viral attachment via the angiotensin-converting enzyme 2 (ACE2) receptor. A unique three-residue RGD motif outside the ACE2 recognition site may allow the spike protein to bind to endothelial proteins called integrins, that bind the RGD group.
In fact, the major integrin on endothelial cells, called αVβ3, is able to bind to multiple RGD-binding ligands. It also engages multiple extracellular matrix proteins, such as fibrinogen, fibronectin, and vitronectin, via its binding pocket. These matrix proteins regulate cell adhesion, migration, and proliferation, as well as angiogenesis.
This mutation could thus enhance SARS-CoV-2 binding to the host cell and may be responsible for the high transmissibility of this virus compared to the earlier ones, while also allowing for multiple routes of entry for the virus and promoting its dissemination within the host by two receptors.
SARS-CoV-2 thus produces marked dysregulation of the endothelial barrier, causing it to lose its integrity and producing a hyper-permeable state. This leads to shock and the rapid spread of the virus to major organs.
Endothelial cells are key to several physiological processes including activation of immune cells, platelet aggregation and adhesion, leukocyte adhesion, and transmigration. They are also the target of many viruses, leading to multi-organ dysfunction.
Some studies have failed to show the growth of the virus within endothelial cells, which has been attributed to the lack of expression of the angiotensin-converting enzyme 2 (ACE2) receptor on these cells.
However, it may be argued that this is due to the intrinsic differences between the endothelial monolayer grown in vitro, vs the endothelial lining of the blood vessels that handle blood flowing under shear stress; the activation of the endothelial cells by the high volume of cytokines; and the tight contact with the epithelial cells of the lung capillaries.
Other researchers have reported that SARS-CoV-2 is found in association with the endothelial cell marker CD31 within the lungs, in infected mice and non-human primates (NHPs). Even more significantly, this finding has been identified in the lung tissue of people who died of severe COVID-19.
The viral proteins were also found in endothelial cells. Moreover, infected mice showed upregulated KRAS signaling pathways in lung tissue, known to mediate cellular activation and dysfunction. Experimental evidence shows that mouse endothelial cells are infected by SARS-CoV-2.
Though all endothelial cells express ACE2, all are not the targets of the virus. Instead, it requires the co-expression of other host proteases such as the transmembrane serine protease TMPRSS2, or cathepsins, that cleave the spike protein to its fusion conformation, allowing viral entry into the host cell via endocytosis.
Following the viral entry into the endothelial cell, it begins to translate its proteins, replicate itself, and may directly induce cell injury and apoptosis. Along with this, endothelial cells activate T cells, though less than other antigen-presenting cells do. In fact, endothelial cells activate only antigen-specific memory or effector T cells, not naïve lymphocytes.
In so doing, endothelial cells may promote the destruction of infected cells by presenting viral proteins to CD8 T cells. Moreover, endothelial cells in the microvasculature may cause memory or effector CD4 T cells to migrate through the endothelium. Antiviral cytokines including gamma-interferon (IFN-γ) may induce class I or II major histocompatibility complex (MHC) molecules, costimulatory molecules that are typically required for T cell activation to occur.
This means that the endothelial dysfunction caused by COVID-19 blocks lymphocyte activation via endothelial cells, causing an imbalance in the adaptive immune response.
The cytokine storm leads to a kind of overreach, causing further endothelial dysfunction. These cytokines include interleukin-6 (IL-6) that stimulates endothelial cell secretion of pro-inflammatory mediators and complement activation, thus further enhancing endothelial barrier breakdown.
Lymphocyte depletion often seen in COVID-19 could also be the result of the excessive inflammation induced by the endothelial cell injury. The reduced number of CD4 lymphocytes may cause an impaired response to the infection while also stimulating further inflammation. Thus, the hyper-inflammatory response in severe and critical COVID-19 could be due to endothelial cell infection and dysfunction.
SARS-CoV-2 infection causes immune dysfunction as well as extensive endothelial injury, in addition to clotting defects and systemic microangiopathy. The poor disease outcome is mediated largely through the increased vascular permeability secondary to infection-related inflammation.
This hyper-permeability is associated with the leakage of both cellular and non-cellular components of the blood in the small blood vessels of the lung, causing the alveoli to become congested with liquid. The patient drowns in the fluid from the leaky blood vessels, which can endanger life by causing asphyxiation.
Simultaneously, the clotting cascades are dysregulated, causing microthrombi to form throughout the circulation, along with leukocyte infiltration. The endothelial cell dysfunction may cause further inflammation and leukocyte recruitment and adhesion.
Since endothelial cells express glycosaminoglycans and thrombomodulin on their cell surface, they inhibit the clotting cascade component, thrombin, as well as a protein inhibitor of tissue factor. Many relaxing factors such as nitric oxide (NO) and prostacyclin (PGI2) are also produced by these cells, thus blocking leukocyte and platelet adhesion and migration, smooth muscle proliferation, and exerting an anti-inflammatory, anti-apoptotic effect.
When the endothelial cells are injured by the viral invasion, they cease to exert their anticoagulant effect, leading to a thrombotic tendency that manifests as extensive microthrombi, hyaline membrane formation in the small arterioles of the lung, and diffuse alveolar injury.
Elevated D-dimer levels occur with this hypercoagulable state, causing poor outcomes and higher mortality with COVID-19. Multiple procoagulant mechanisms are at work, from the exposure of the tissue factor to clotting factors in the blood to the loss of endothelial integrity and thus activation of the intrinsic clotting pathway by the exposed matrix under the endothelial cell layer, to the devastating release of van Willebrand factor (vWF), due to endothelial dysfunction. This molecule acts to bridge platelets for aggregation and clot formation.
Infection of the endothelial cells could be associated with viral invasion of the adjacent tissues, that is, of the smooth muscle cells of the arteries and the cardiac myocytes.
Thus, SARS-CoV-2 infection of endothelial cells could be an underlying cause for the cardiovascular complications of COVID-19, including the end-stage multi-organ dysfunction. It is plausible that the endothelial cell apoptosis was seen in patients who have died of COVID-19, as well as the microthrombi scattered throughout the lung vascular bed along with right ventricular dysfunction, are associated with direct infection of the endothelial cells.
The binding of the spike protein to αVβ3 can be inhibited by the specific αVβ3-antagonist Cilengitide, an RGD tripeptide, that has a high affinity to this integrin and suppresses virus-endothelium binding at very low doses.
Other therapeutic strategies include serine protease inhibitors, renin-angiotensin-aldosterone system inhibitors, statins, heparin, corticosteroids, and IL-6 inhibitors, all of which act at least in part via stabilization and protection of endothelial integrity.
Last Updated: Oct 27, 2021
Written by
Dr. Liji Thomas is an OB-GYN, who graduated from the Government Medical College, University of Calicut, Kerala, in 2001. Liji practiced as a full-time consultant in obstetrics/gynecology in a private hospital for a few years following her graduation. She has counseled hundreds of patients facing issues from pregnancy-related problems and infertility, and has been in charge of over 2,000 deliveries, striving always to achieve a normal delivery rather than operative.
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HIF-1α promotes the proliferation and migration of pulmonary arterial smooth muscle cells via activation of Cx43 – DocWire News

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J Cell Mol Med. 2021 Oct 26. doi: 10.1111/jcmm.17003. Online ahead of print.
The proliferation of pulmonary artery smooth muscle cells (PASMCs) is an important cause of pulmonary vascular remodelling in hypoxia-induced pulmonary hypertension (HPH). However, its underlying mechanism has not been well elucidated. Connexin 43 (Cx43) plays crucial roles in vascular smooth muscle cell proliferation in various cardiovascular diseases. Here, the male Sprague-Dawley (SD) rats were exposed to hypoxia (10% O2 ) for 21 days to induce rat HPH model. PASMCs were treated with CoCl2 (200 µM) for 24 h to establish the HPH cell model. It was found that hypoxia up-regulated the expression of Cx43 and phosphorylation of Cx43 at Ser 368 in rat pulmonary arteries and PASMCs, and stimulated the proliferation and migration of PASMCs. HIF-1α inhibitor echinomycin attenuated the CoCl2 -induced Cx43 expression and phosphorylation of Cx43 at Ser 368 in PASMCs. The interaction between HIF-1α and Cx43 promotor was also identified using chromatin immunoprecipitation assay. Moreover, Cx43 specific blocker (37,43 Gap27) or knockdown of Cx43 efficiently alleviated the proliferation and migration of PASMCs under chemically induced hypoxia. Therefore, the results above suggest that HIF-1α, as an upstream regulator, promotes the expression of Cx43, and the HIF-1α/Cx43 axis regulates the proliferation and migration of PASMCs in HPH.
PMID:34698450 | DOI:10.1111/jcmm.17003