thermoregulatory dysfunction in covid 19

7). Researchers from the University of Milan, Italy have found a link between thyroid dysfunction and moderate-to-severe COVID-19. volume44,pages 695709 (2023)Cite this article. Direct or indirect mechanisms are operating to collectively indicate the alterations in vascular homeostasis in COVID-19 [54]. Zha D, Fu M, Qian Y. Vascular endothelial glycocalyx damage and potential targeted therapy in COVID-19. Circ Res. The authors observed elevated levels of markers of coagulopathy/endotheliopathy and liver injury (ALT) in COVID-19 patients. Diabetes/hyperglycemia further exacerbate pre-existing endothelial dysfunction and hyperinflammation in COVID-19 patients. QJM. Furthermore, HIVC in combination with other drugs such as giammonium glycyrrhizinate, decreased the incidence rate of ARDS in COVID-19 patients [158]. Dexamethasone treated group exhibited a significantly decreased levels of various markers associated with endothelial dysfunction, including Ang-2, ICAM-1, and sRAGE [135]. Tomasa-Irriguible TM, Bielsa-Berrocal L. COVID-19: Up to 82% critically ill patients had low vitamin C values. Shao Y, Saredy J, Xu K, Sun Y, Saaoud F, Drummer CT, et al. 2020;222:178993. To obtain 2020;116:166687. Further identification of alternative receptors for SARS-CoV-2 is warranted [51]. Kondo Y, Larabee JL, Gao L, Shi H, Shao B, Hoover CM, et al. Huet T, Beaussier H, Voisin O, Jouveshomme S, Dauriat G, Lazareth I, et al. The protective role of ACE2 agonism in suppressing angiogenesis and maintaining endothelial integrity in COVID-19 warrant further investigation [19]. Hussain M, Khurram Syed S, Fatima M, Shaukat S, Saadullah M, Alqahtani AM, et al. Zhang L, Zhou L, Bao L, Liu J, Zhu H, Lv Q, et al. 2021;95:e0079421. 2022;17:30. Contemporary definition of endothelial dysfunction has been extended to a constellation of cellular events including oxidative stress, inflammation/leukocyte adhesion, EndoMT, mitochondria dysfunction, senescence and deregulated endothelial cell metabolism [15]. 2021;8:648290. The vascular endothelium, the innermost layer of blood vessels, provides a dynamic interface between the circulating blood and various tissues/organs and thereby maintaining tissue homeostasis. 2. Direct SARS-CoV-2 infection or indirect effect arising from SARS-CoV-2 infection leads to endothelial dysfunction in pan-vasculature, which results in the development of multi-organ tissue injury. 2021;348:109657. SARS-CoV-2 infection primarily affects the pulmonary system, but accumulating evidence suggests that it also affects the pan-vasculature in the extrapulmonary systems by directly (via virus infection) or indirectly (via cytokine storm), causing endothelial dysfunction (endotheliitis, endothelialitis and endotheliopathy) and multi-organ injury. Free Radic Biol Med. Medications to protect and/or restore the endothelial glycocalyx integrity hold great therapeutic potential for COVID-19 associated glycocalyx disruption. Stahl K, Brsen JH, Hoeper MM, David S. Direct evidence of SARS-CoV-2 in gut endothelium. Management includes warming measures, hydration, and cardiovascular support. Direct activation of endothelial cells by SARS-CoV-2 nucleocapsid protein is blocked by simvastatin. The fight against coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 infection is still raging. Here, we reviewed the potential mechanism of endothelial activation in COVID-19 by overviewing the most recent literature, with the aim to provide targeted therapies (Fig. 2022;23:6196. Kang S, Tanaka T, Inoue H, Ono C, Hashimoto S, Kioi Y, et al. Sansone A, Jannini EA. Fang W, Jiang J, Su L, Shu T, Liu H, Lai S, et al. 2021;599:2839. 2021;95:e0139621. 2021;11:937696. 2022. https://doi.org/10.21203/rs.3.rs-1762855/v1. However, the NPs from other coronaviruses such as Middle East respiratory syndrome coronavirus, SARS-CoV and H1N1 fail to cause endothelial activation, echoing the observation of endotheliitis, vasculopathy and coagulopathy in severe COVID-19 patients [45]. Interferon-alpha or -beta facilitates SARS-CoV-2 pulmonary vascular infection by inducing ACE2. A significant proportion of people who test positive for COVID-19 have chemosensory deficits. Cardiovasc Res. Cytokine storm in COVID-19 can trigger inflammation via the JAK/STAT pathway, which results in increased recruitment of leukocytes/immune cells [146]. In addition to the above-mentioned organ injuries, COVID-19 also leads to neuropathy [39], redox imbalance and mitochondria dysfunction which may underlie neurological complications of COVID-19 [40]. Thermoregulation is a vital function of the autonomic nervous system in response to cold and heat stress. Chen S, Zheng C, Chen T, Huang D, Pan Y, Chen S. Relationship between plasma vitamin C and COVID-19 susceptibility and severity: a two-sample mendelian randomization study. Meyer K, Patra T, Vijayamahantesh, Ray R. SARS-CoV-2 spike protein induces paracrine senescence and leukocyte adhesion in endothelial cells. Food Chem Toxicol. 2021;47:3929. 2017BT01S131), Hefei Comprehensive National Science Center (Grant No. J Inflamm Res. Colchicine is an ancient and low-cost drug isolated from Chinese herbal medicine. TCM has a well-documented safety profile in protecting against COVID-19 on the basis of standard care. The IL-1, IL-6, and TNF cytokine triad is associated with post-acute sequelae of COVID-19. COVID-19-Associated lung microvascular endotheliopathy: a from the bench perspective. Article Both SARS-CoV and SARS-CoV-2 utilizes ACE2 and membrane-bound co-factors for virus entry. 2021;45:11639. 2015 Sep;39(3):139-48. doi: 10.1152/advan.00126.2014. 2020;24:422. Okada H, Yoshida S, Hara A, Ogura S, Tomita H. Vascular endothelial injury exacerbates coronavirus disease 2019: The role of endothelial glycocalyx protection. Pine AB, Meizlish ML, Goshua G, Chang CH, Zhang H, Bishai J, et al. The polypharmacological profile of metformin makes it a promising candidate drug to be repurposed for controlling inflammation tsunami in diabetic COVID-19 patients [124]. Signal Transduct Target Ther. 2) [2, 16]. Front Med. Based on these protective effects, statin may be used as an adjunctive therapy to mitigate endothelial dysfunction accompanying SARS-CoV-2 infection. Angpt-2 angiopoietin-2, CCL2 chemokine (C-C motif) ligand 2, ECs endothelial cells, FMD flow-mediated dilation, HMWM high-molecular-weight multimers, IL-1 interleukin-1, IL-6 interleukin 6, PDGF-BB platelet-derived growth factor BB, s-Flt soluble fms-like tyrosine kinase, sICAM1 soluble ICAM1, sVCAM1 soluble VCAM1, sVE-cadherin soluble vascular endothelial cadherin, TF tissue factor, TNF- tumor necrosis factor, VEGF-A vascular endothelial growth factor A, vWF von Willebrand factor. Thus, COVID-19 is deemed as a (micro)vascular and endothelial disease. The Erectile Dysfunction Drugs report tracks competitive progresses, strategies, mergers and acquisitions and new product development. 2020;98:31422. Recent studies have suggested that LSEC dysfunction is involved in COVID-19 associated liver injury [34]. 2021;63:103182. Ni L, Wen Z, Hu X, Tang W, Wang H, Zhou L, et al. Mitochondria is an important organelle that regulates antioxidant/redox signaling, by fine-tuning mitochondria-derived reactive oxygen species (mtROS) production. A meta-analysis revealed the favorable effect of statins in COVID-19 patients [118]. The following is a summary of "Optimal positive end-expiratory pressure reduces right ventricular dysfunction in COVID-19 patients on venovenous extracorporeal membrane oxygenation: A retrospective single-center study," published in the February 2023 issue of Critical Care by Estoos et al. These include tachycardia, shortness of breath, fatigue and post-exercise exhaustion. It is noted that even in convalescent COVID-19 patients undergoing rehabilitation, cognitive impairment and endothelial dysfunction still exist, indicating the necessity to monitor endothelial dysfunction in convalescent patients [42]. Several large-scale clinical trials have suggested that glucocorticoid drug dexamethasone treatment is beneficial for COVID-19 patients [134]. 2022;17:e0268296. QJM. The Sexual Long COVID (SLC): Erectile Dysfunction as a Biomarker of Systemic Complications for COVID-19 Long Haulers - PubMed. J Thrombosis Haemost. Google Scholar. Plasma level of resistin is increased in COVID-19 patients and associated with disease severity as well as the expression of inflammatory cytokines (IL-6, IL-8 and MCP-1) and adhesion molecules (ICAM1 and VCAM1) [80]. Phytother Res. Ma S, Sun S, Li J, Fan Y, Qu J, Sun L, et al. In addition to mtROS, other sources of ROS can also be possible, such as ROS derived from NADPH oxidase activation as well as eNOS uncoupling [85]. Published: April 28, 2023 at 7:55 a.m. Excessive production of mtROS causes oxidative stress that perpetuates ECs inflammation, senescence and dysfunction. EBioMedicine. Recent studies have demonstrated that complement activation is associated with SARS-CoV-2 infection induced inflammation, endothelial injury, hypercoagulability and thrombosis [95]. These data agree with recent report of the clinical benefits of statin therapy in lowering the risk of mortality of COVID-19 [119]. 2021;7:9. Intern Emerg Med. ACE2 is highly expressed in many major organs/tissues, including the heart, lung, kidneys. Joffre J, Rodriguez L, Matthay ZA, Lloyd E, Fields AT, Bainton RJ, et al. Han T, Ma S, Sun C, Zhang H, Qu G, Chen Y, et al. In addition, COVID-19 is an important risk factor for developing acute myocardial infarction [29]. COVID-19 and Endothelial Cell Dysfunction Initial SARS-CoV-2 infection occurs within the lung epithelia, whereby serine proteases, most notably transmembrane protease serine 2 (TMPRSS2), cathepsin B, and cathepsin L1, prime the SARS-CoV-2 spike glycoprotein, which is followed by ACE2-mediated viral entry ( 29 ). It has been recently reviewed that restoration of balanced effects between the RAAS and ACE2/Ang-(17)/MAS could be a promising way to ameliorate multi-organ injury associated with COVID-19 [130]. 2020;202:117881. Mol Neurobiol. Acute myocardial infarction in the Covid-19 era: Incidence, clinical characteristics and in-hospital outcomes-A multicenter registry. world J mens health. Torices S, Motta C, da Rosa B, Marcos A, Alvarez-Rosa L, Siqueira M, et al. The American-European Consensus Conference definition of the acute respiratory distress syndrome is dead, long live positive end-expiratory pressure! Article SARS-CoV-2 infects the ECs and epithelial cells in lung tissues via angiotensin-converting enzyme-2 (ACE2) and alternative receptors [21] on host cells [22]. Mechanistic studies in cultured human ECs suggest that COVID-19 induced endothelial inflammation and monocyte adhesion was ameliorated by atorvastatin and KLF2 overexpression, suggesting the possible utility of KLF2 activator in suppressing COVID-19 associated endothelial dysfunction [120]. Arteriosclerosis Thrombosis Vasc Biol. Redox Biol. The PubMed wordmark and PubMed logo are registered trademarks of the U.S. Department of Health and Human Services (HHS). In light of the multiple endothelial protective effects exerted by SGLT2 inhibitors [127], this type of drug hold promises to treat COVID-19 patients with T2DM. The pleiotropic effects of metformin help to control hyperglycemia, inhibit viral entry, and reduce inflammation following SARS-CoV-2 infection. Elevated expression of serum endothelial cell adhesion molecules in COVID-19 patients. Vasc Pharmacol. Signal Transduct Target Ther. An important question in endothelial dysfunction caused by SARS-Co-V2 is whether SARS-CoV-2 can infect and cause (passively or actively) endothelial dysfunction and long COVID [7]. Am J Respiratory Cell Mol Biol. The levels of senescent markers, such as PAI-1, p21 and sirtuin-1 in the plasma and lung ECs are elevated. A review of acute limb ischemia in COVID-positive patients. 2022;13:830061. ACE2 is an important component of the renin-angiotensin-aldosterone system (RAAS) by converting vasoactive AngII into Ang (17). In addition, the levels of these endothelial markers are elevated in intensive care units (ICU) non-survivors compared to survivors. Endothelial dysfunction in COVID-19: a unifying mechanism and a potential therapeutic target. 2020;18:23919. The intact barrier structure of sulfated glycocalyx of the endothelium could repel SARS-CoV-2. Infection with various types of viruses, including SARS-CoV-2, can trigger endothelial senescence. Int J Mol Sci. In addition, spike protein S1-mediated elevation of markers of endothelial inflammation and injury (including E-selectin, ICAM-1, VCAM-1 and PAI-1) and THP-1 monocyte adhesion to ECs was further exacerbated by dihydrotestosterone or TNF- treatment, but ameliorated by spironolactone treatment [77]. Risk of acute myocardial infarction and ischaemic stroke following COVID-19 in Sweden: a self-controlled case series and matched cohort study. It represents a potential biomarker for monitoring disease progression in COVID-19 patients [112]. The infected cell releases danger signals leading to multiple aspects of endothelial dysfunction, which finally leads to impaired vascular activity and multi-organ injury. Introduction IL-1 is an important cytokine released during cytokine storm in COVID-19 as well as its post-acute sequelae [91, 139]. Colunga Biancatelli RML, Solopov PA, Sharlow ER, Lazo JS, Marik PE, Catravas JD. Keywords: COVID-19; heat plan; heat stress; pandemic; personal protective equipment; sars-CoV-2; thermometry. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Mitochondrial DNA and TLR9 activation contribute to SARS-CoV-2-induced endothelial cell damage. Cell Biosci. Deaths from . Endothelial cells are sentinels lining the innermost layer of blood vessel that gatekeep micro- and macro-vascular health by sensing pathogen/danger signals and secreting vasoactive molecules. Thus, hyperinflammation and inflammasome activation associated with SARS-CoV-2 infection will lead to endothelial cell injury and death (such as pyroptosis). Complement activation induces excessive T cell cytotoxicity in severe COVID-19. J Virol. Arteriosclerosis Thrombosis Vasc Biol. PLoS One. 2021;9:639. 2022;9:844228. Falleni M, Tosi D, Savi F, Chiumello D, Bulfamante G. Endothelial-mesenchymal transition in COVID-19 lung lesions. N Engl J Med. Microcirculation (N. Y, N. Y: 1994). Clin Transl Immunol. COVID-19-associated coagulopathy (CAC) is a life-threatening complication of SARS-CoV-2 infection. Am J Respiratory Crit Care Med. Satarker S, Tom AA, Shaji RA, Alosious A, Luvis M, Nampoothiri M. JAK-STAT pathway inhibition and their implications in COVID-19 therapy. CAS Jothimani D, Venugopal R, Abedin MF, Kaliamoorthy I, Rela M. COVID-19 and the liver. In a single-center observational study, 82% of critically ill COVID-19 patients have significantly lower plasma level of vitamin C [154]. doi: 10.1097/MD.0000000000033345. Pawlos A, Niedzielski M, Gorzelak-Pabi P, Broncel M, Woniak E. COVID-19: direct and indirect mechanisms of statins. eCollection 2023 Apr. Amraei R, Yin W, Napoleon MA, Suder EL, Berrigan J, Zhao Q, et al. Human lung microvascular endothelial cells (HLMVEC) are activated after infection with the S1 protein or S1 infected human macrophages, evidenced by increased expression of pro-coagulant marker (tissue factor), and cytokines/chemokines (ICAM-1, VCAM-1 and MCP1) [54]. Avoidance of thermal risk and early recognition of cold or heat stress are the cornerstones of preventive therapy. COVID19 has infected at least 25,248,595 persons worldwide through August 31, 2020, causing 846,877 deaths. 2020;383:225573. In this regard, ACE2 downregulation and the disrupted balance between the RAAS and ACE2/Ang-(17)/MAS axis may also contribute to multiple organ injury in COVID-19 [87, 130]. Plasma from COVID-19 patients triggered glycocalyx shedding and disruption in endothelial cells, which can be prevented after treatment with heparin [66]. 2021;142:106946. Br J Pharmacol. Liver injury in COVID-19 and IL-6 trans-signaling-induced endotheliopathy. In cultured endothelial cells, patient plasma also induced glycocalyx shedding and ROS production, which can be prevented by low molecular weight heparin [66]. It is well-known that IL-1 induces the expression of itself and other pro-inflammatory and pro-adhesive molecules, such as TNF-, leading to the amplification of cytokine storm. Xing D, Liu Z. HIVC improves myocardial injury via decreasing biomarkers associated with inflammation in critically ill COVID-19 patients [155]. 2022: 1-10. 82070464, 81941022, 81530025) and Strategic Priority Research Program of Chinese Academy of Sciences (Grant No. Sci Immunol. This study highlights the crucial role of IL-6 trans-signaling in endothelial dysfunction/endotheliopathy in COVID-19 [137]. In addition, S1 subunit of SARS-CoV-2 spike protein (S1) decreased endothelial barrier function in cultured human pulmonary microvascular ECs [22]. We also present emerging therapeutic agents and therapeutic targets which are directed at reducing the consequence of endothelial dysfunction/endotheliitis/endotheliopathy. Lopes-Paciencia S, Saint-Germain E, Rowell MC, Ruiz AF, Kalegari P, Ferbeyre G. The senescence-associated secretory phenotype and its regulation. Lee KCH, Sewa DW, Phua GC. In support of this finding, significantly higher level of angiogenesis was observed in lung tissues from COVID-19 patients, compared with patients with influenza [83]. Front Med. A recent multi-omics study has revealed that COVID-19 associated AKI resembles AKI induced by sepsis, which involves the mechanism of mitochondria dysfunction, inflammation, necroptosis, capillary congestion and endothelial injury [37]. Abraham GR, Kuc RE, Althage M, Greasley PJ, Ambery P, Maguire JJ, et al. ECs are also capable of counteracting ROS, by increasing superoxide dismutase (SOD), catalase, glutathione peroxidase, and NRF2-dependent heme-oxygenase 1 expression [2]. J Intern Med. Targeting endothelial dysfunction in eight extreme-critically ill patients with COVID-19 using the anti-adrenomedullin antibody adrecizumab (HAM8101). Moreover, supernatant from virus-infected cells can trigger neutrophil extracellular trap formation and platelet activation [88]. eLife. Nagashima S, Mendes MC, Camargo Martins AP, Borges NH, Godoy TM, Miggiolaro A, et al. Resistin is peptide hormone derived from adipose tissue which is associated with endothelial injury and inflammatory response. Pharmacol Res. 2023;17(9):105. doi: 10.1007/s11783-023-1705-1. One universal mechanism of endothelial inflammation in COVID-19 patients is plausibly associated with the downregulation of KLF2 [81], a master regulator of vascular homeostasis. 2021;27:151. Extrapulmonary manifestations of COVID-19. Of translational significance, COVID-19 patients derived serum also increased mtDNA release in ECs, compared to control subjects. Increased endothelial inflammation evidenced by the increased expression of various cytokines/adhesion molecules is a classical instance of endothelial dysfunction. CAS Flaumenhaft R, Enjyoji K, Schmaier AA. Corrao S, Pinelli K, Vacca M, Raspanti M, Argano C. Type 2 diabetes mellitus and COVID-19: a narrative review. Use the Previous and Next buttons to navigate the slides or the slide controller buttons at the end to navigate through each slide. Won T, Wood MK, Hughes DM, Talor MV, Ma Z, Schneider J, et al. Adv Physiol Educ. However, statin use can also induce the expression of ACE2, which may potentially increase virus entry [117]. High-dose intravenous vitamin C decreases rates of mechanical ventilation and cardiac arrest in severe COVID-19. 01 May 2023 01:18:34 MacKenzie MA, Hermus AR, Wollersheim HC, Binkhorst RA, Pieters GF. Acute brain dysfunction is highly prevalent in COVID-19 patients. Cytokine storm. April 27, 2023 - A new study shows that people with long COVID respond differently to COVID vaccines and that the condition may be caused by a dysfunction of the immune system -- possibly . 5. Data from multi-center registry support that ST-segment elevation myocardial infarction (STEMI) patients enrolled during the first-wave of COVID-19 experience longer time of ischemia and a higher rate of adverse events [30, 31], suggesting the need for COVID-19 vaccines. The fight against coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 infection is still raging.

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