The potential role of ischaemia–reperfusion injury in chronic, relapsing diseases such as rheumatoid arthritis, Long COVID, and ME/CFS: evidence, mechanisms, and therapeutic implications

Biochemical Journal, Journal Year: 2022, Volume and Issue: 479(16), P. 1653 - 1708

Published: Aug. 31, 2022

Ischaemia-reperfusion (I-R) injury, initiated via bursts of reactive oxygen species produced during the reoxygenation phase following hypoxia, is well known in a variety acute circumstances. We argue here that I-R injury also underpins elements pathology chronic, inflammatory diseases, including rheumatoid arthritis, ME/CFS and, our chief focus and most proximally, Long COVID. Ischaemia may be fibrin amyloid microclot blockage capillaries, for instance as exercise started; reperfusion necessary corollary when it finishes. rehearse mechanistic evidence these occurrences here, terms their manifestation oxidative stress, hyperinflammation, mast cell activation, production marker metabolites related activities. Such microclot-based phenomena can explain both breathlessness/fatigue post-exertional malaise observed conditions, many other observables. The recognition processes implies, mechanistically, therapeutic benefit potentially to had from antioxidants, anti-inflammatories, iron chelators, suitable, safe fibrinolytics, and/or anti-clotting agents. review considerable existing consistent with this, biochemical mechanisms involved.

Language: Английский

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The intersection of obesity and (long) COVID-19: Hypoxia, thrombotic inflammation, and vascular endothelial injury

Frontiers in Cardiovascular Medicine, Journal Year: 2023, Volume and Issue: 10

Published: Feb. 7, 2023

The role of hypoxia, vascular endothelial injury, and thrombotic inflammation in worsening COVID-19 symptoms has been generally recognized. Damaged endothelium plays a crucial forming situ thrombosis, pulmonary dysfunction, hypoxemia. Thrombotic can further aggravate local injury affect ventilation blood flow ratio. According to the results many studies, obesity is an independent risk factor for variety severe respiratory diseases contributes high mechanical rate, mortality, slow recovery patients. This review will explore mechanisms by which may acute phase delay long COVID affecting inflammation. A systematic search PubMed database was conducted papers published since January 2020, using medical subject headings "COVID-19" "long COVID" combined with following keywords: "obesity," "thrombosis," "endothelial injury," "inflammation," "hypoxia," "treatment," "anticoagulation." In patients obesity, accumulation central fat restricts expansion alveoli, exacerbating dysfunction caused SARS-CoV-2 invasion, inflammatory damage, lung edema. Abnormal secretion immune impairment original tissue damage diffusion. Obesity weakens baseline function leading early pre-thrombotic state after infection. Enhanced procoagulant activity microthrombi promote obstruction vascular. also prolongs duration increases sequelae hospital discharge. Persistent viral presence, long-term inflammation, microclots, hypoxia contribute development persistent symptoms, suggesting that are uniquely susceptible COVID. Early interventions, including supplemental oxygen, comprehensive antithrombotic therapy, anti-inflammatory drugs, show effectiveness studies prevention serious thromboembolic events, systemic therefore recommended reduce intensive care unit admission, sequelae.

Language: Английский

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Prevalence and risk factors for long COVID and post-COVID-19 condition in Africa: a systematic review

The Lancet Global Health, Journal Year: 2023, Volume and Issue: 11(11), P. e1713 - e1724

Published: Oct. 17, 2023

An improved estimation of the clinical sequelae SARS-CoV-2 infection is crucial in African countries, where subject has received little attention despite more than 12 million reported cases and evidence that many people were infected. We reviewed on prevalence, associated risk factors for long COVID, systemic or sociocultural determinants reporting COVID.

Language: Английский

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Multimodal Molecular Imaging Reveals Tissue-Based T Cell Activation and Viral RNA Persistence for Up to 2 Years Following COVID-19

medRxiv (Cold Spring Harbor Laboratory), Journal Year: 2023, Volume and Issue: unknown

Published: July 31, 2023

ABSTRACT The etiologic mechanisms of post-acute medical morbidities and unexplained symptoms (Long COVID) following SARS-CoV-2 infection are incompletely understood. There is growing evidence that viral persistence immune dysregulation may play a major role. We performed whole-body positron emission tomography (PET) imaging in cohort 24 participants at time points ranging from 27 to 910 days acute using novel radiopharmaceutical agent, [ 18 F]F-AraG, highly selective tracer allows for anatomical quantitation activated T lymphocytes. Tracer uptake the COVID group, which included those with without Long symptoms, was significantly higher compared pre-pandemic controls many regions, including brain stem, spinal cord, bone marrow, nasopharyngeal hilar lymphoid tissue, cardiopulmonary tissues, gut wall. Although cell activation tended be imaged closer illness, increased up 2.5 years infection. observed cord wall associated presence symptoms. In addition, lung tissue persistent pulmonary Notably, these tissues also individuals COVID. Given high F]F-AraG detected gut, we obtained colorectal situ hybridization RNA immunohistochemical studies subset identified cellular rectosigmoid lamina propria all participants, 158 676 initial COVID-19 suggesting could long-term immunological perturbations.

Language: Английский

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Long COVID-19 Pathophysiology: What Do We Know So Far?

Microorganisms, Journal Year: 2023, Volume and Issue: 11(10), P. 2458 - 2458

Published: Sept. 30, 2023

Long COVID-19 is a recognized entity that affects millions of people worldwide. Its broad clinical symptoms include thrombotic events, brain fog, myocarditis, shortness breath, fatigue, muscle pains, and others. Due to the binding virus with ACE-2 receptors, expressed in many organs, it can potentially affect any system; however, most often cardiovascular, central nervous, respiratory, immune systems. Age, high body mass index, female sex, previous hospitalization, smoking are some its risk factors. Despite great efforts define pathophysiology, gaps remain be explained. The main mechanisms described literature involve viral persistence, hypercoagulopathy, dysregulation, autoimmunity, hyperinflammation, or combination these. exact may differ from system system, but share same pathways. This review aims describe prevalent pathophysiological pathways explaining this syndrome.

Language: Английский

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