2021;185:106469. The glycocalyx is a proteoglycan- and glycoprotein-rich microstructure covering ECs essential for maintaining vascular homeostasis via regulating vascular tone, permeability, thrombosis and leukocyte adhesion to endothelium [66]. A systematic review was conducted by searching MEDLINE, EMBASE, and the preprint server MedRxiv from their inception until May 11, 2020, using the terms anosmia or hyposmia or dysosmia or olfactory dysfunction or olfaction disorder or smell dysfunction or ageusia or hypogeusia or dysgeusia or taste dysfunction or gustatory dysfunction or neurological and COVID-19 or 2019 novel coronavirus or . Under physiological conditions, ECs undergoing apoptotic process are released into circulating blood. Cecon E, Fernandois D, Renault N, Coelho CFF, Wenzel J, Bedart C, et al. Glycocalyx degradation and shedding disrupts endothelial junctional stability and plays a pivotal role in various forms of cardiovascular diseases [111]. eCollection 2023 Apr. Corrao S, Pinelli K, Vacca M, Raspanti M, Argano C. Type 2 diabetes mellitus and COVID-19: a narrative review. Virus-induced senescence is a pathogenic trigger of endothelial dysfunction. Circulating level of Angiopoietin-2 is associated with acute kidney injury in coronavirus disease 2019 (COVID-19). The https:// ensures that you are connecting to the "Persisting pulmonary dysfunction in pediatric post-acute Covid-19" "Our study demonstrates widespread functional lung alterations are present in children and adolescents." 30 Apr 2023 18:49:04 Front Med. Ice water immersion has been shown to be superior to alternative cooling measures. Front Pharmacol. EC depletion from the luminal surface reduces NO production and impair endothelium-dependent vasorelaxation [20]. Nagashima S, Mendes MC, Camargo Martins AP, Borges NH, Godoy TM, Miggiolaro A, et al. SARS-CoV-2 targets the pulmonary system, as well as the extrapulmonary system [2]. Eur J Clin Invest. mydriasis, hypotension, and muscle dysfunction, which can progress to cardiac arrest or coma. Syndecan-1, an important vascular component of glycocalyx released after vasculitis and injury, well correlates with the marker of coagulation (D-dimer) in particular. Li F, Li J, Wang PH, Yang N, Huang J, Ou J, et al. A retrospective study in COVID-19 patients with pre-existing T2DM indicated that metformin treatment was associated with the occurrence of acidosis as well as reduced heart failure and inflammation. 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]. Emerging evidence has suggested that thinning of endothelial glycocalyx layer is associated with COVID-19, and thus the glycocalyx integrity was perceived as an important therapeutic target in COVID-19 [109, 110]. The levels of biomarkers of endothelial cell activation/injury well correlate with the expression level of pro-inflammatory cytokines and chemokines [103]. 2022; 2090792. https://doi.org/10.1080/21688370.2022.2090792. Acta Pharmacol Sin 44, 695709 (2023). Front Med. 2020;75:e1980. Targeting inflammation and cytokine storm in COVID-19. Chin Med. Mitochondrial dysfunction usually occurs after viral infection, thereby exacerbating tissue damage. Poloni TE, Medici V, Moretti M, Vison SD, Cirrincione A, Carlos AF, et al. A recent study has shown that SARS-CoV-2-infection of human brain microvascular ECs showed augmented caspase 3 cleavage and apoptotic cell death of endothelial cells. Among these physiological functions, nitric oxide (NO) represents the key mechanism for maintaining endothelial homeostasis [2, 15]. The net consequence is the extravasation of inflammatory and immune cell infiltrations [74]. It is well-established that SARS-CoV-2 enters host cells including ECs via ACE2 and coreceptor TMPRSS2. Anakinra for severe forms of COVID-19: a cohort study. 2020;24:422. 4 and 5) [101]. Introduction 2021;290:43743. 2020;5:e138070. 2020;145:111694. 2021;348:109657. ACE2 is an important component of the renin-angiotensin-aldosterone system (RAAS) by converting vasoactive AngII into Ang (17). In this study we assessed both olfaction and gustation using psychophysical tests eight months after COVID-19. 3). 2022;115:7783. 2021;375:n2400. Huang Q, Wu X, Zheng X, Luo S, Xu S, Weng J. These vasoactive molecules tightly control the fine balance between vasodilatory and vasoconstrictory, pro-proliferative and anti-proliferative, pro-thrombotic and anti-thrombotic, pro-oxidant and antioxidant, fibrinolytic and anti-fibrinolytic, and pro-inflammatory and anti-inflammatory responses (Fig. Potje SR, Costa TJ, Fraga-Silva TFC, Martins RB, Benatti MN, Almado CEL, et al. Lowenstein CJ, Solomon SD. Qin H, Zhao A. Mesenchymal stem cell therapy for acute respiratory distress syndrome: from basic to clinics. 2022. https://doi.org/10.1164/rccm.202107-1774OC. Extrapulmonary manifestations of COVID-19. Theranostics. It is possible that these cytokines will disrupt the integrity of various types of junctional proteins, including VE-cadherin, ZO-1, -catenin and gap junction proteins. Dexamethasone may improve severe COVID-19 via ameliorating endothelial injury and inflammation: A preliminary pilot study. . 2021;1321:3343. 2020;324:2292300. SARS-CoV-2 leads to a small vessel endotheliitis in the heart. Endothelial cells and SARS-CoV-2: An intimate relationship. EndoMT, defined as the loss of endothelial markers/characteristics (CD31, VE-cadherin and Tie2) and gaining of mesenchymal cell markers (FSP-1, -SMA and vimentin), is central to COVID-19 induced lung fibrosis and pulmonary artery hypertension [72, 73]. 2021;1867:166260. 2022;216:1204. However, there are also reports showing that ACE2 expression is absent from human ECs. Likewise, in a retrospective study involving ninety-nine patients with COVID-19, the degree of endothelial damage was correlated with disease severity in COVID-19, suggesting that number of CEC is a good predictor of disease severity [116]. A number of viral species, such as dengue, ebola and cytomegalovirus can infect endothelial cells (ECs) and cause endothelial dysfunction [5]. Huang P, Zuo Q, Li Y, Oduro PK, Tan F, Wang Y, et al. Sci Transl Med. Stahl K, Gronski PA, Kiyan Y, Seeliger B, Bertram A, Pape T, et al. Amraei R, Rahimi N. COVID-19, Renin-Angiotensin system and endothelial dysfunction. Br J Pharmacol. Thus, COVID-19 is deemed as a (micro)vascular and endothelial disease. Zhang D, Li L, Chen Y, Ma J, Yang Y, Aodeng S, et al. Risk of acute myocardial infarction and ischaemic stroke following COVID-19 in Sweden: a self-controlled case series and matched cohort study. 1) [14]. 2021;13:2090614. Activation of IL-6 trans-signaling in LSECs leads to coagulopathy, elevation of pro-inflammatory factors, and platelet adhesion to LSECs. 2020;159:105051. Endothelial senescence is an important aspect of endothelial dysfunction. 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. Pharmacopsychiatry. Stem Cell Rep. 2021;16:245972. In summary, heat in combination with the COVID-19 pandemic leads to additional problems; the impact of which can be reduced by revising heat plans and implementing special measures attentive to these compound risks. Tomasa-Irriguible TM, Bielsa-Berrocal L. COVID-19: Up to 82% critically ill patients had low vitamin C values. 2021;128:13236. Clin Transl Immunol. Mortality risk among patients with COVID-19 prescribed selective serotonin reuptake inhibitor antidepressants. and JavaScript. ACE inhibitors, angiotensin receptor blockers and endothelial injury in COVID-19. Employing mechanical ventilation techniques on venovenous extracorporeal membrane oxygenation (VV ECMO . Vollenberg R, Tepasse PR, Ochs K, Floer M, Strauss M, Rennebaum F, et al. Lancet Rheumatol. 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. 2022;119:31925. In addition, plasma profiling study of patients with COVID-19 revealed elevated circulating levels of markers of angiogenesis (such as VEGF-A) in COVID-19 patients [84]. Endothelial immunity trained by coronavirus infections, DAMP stimulations and regulated by anti-oxidant NRF2 may contribute to inflammations, myelopoiesis, COVID-19 cytokine storms and thromboembolism. It is reported that COVID-19-patients had higher number of CECs than COVID-19-free subjects. 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]. There are multiple lines of evidences suggesting the involvement of endothelial dysfunction in COVID-19 [45]. 2021;10:e1350. 2022;23:6196. Kidney Int. Senolytic drugs such as navitoclax and quercetin/dasatinib combination selectively eradicated senescent cells and reduced inflammation in SARS-CoV-2-infected animals [89]. Amraei R, Yin W, Napoleon MA, Suder EL, Berrigan J, Zhao Q, et al. Interestingly, the secretion of these cytokines is elevated in COVID-19 patients. Respir Med. Treatment of virus-infected human lung microvascular endothelial cells (HMVECs) with diminazene aceturate (an ACE2 agonist) reverses SARS-CoV-2 infection-induced hyperpermeability, indicating the possibility that ACE2 agonism indeed stabilizes endothelial barrier integrity without affecting viral uptake into ECs [23]. 2021;58:457587. 3). Like other types of cell senescence, virus-induced senescence is associated with senescence-associated secretory phenotype (SASP), which is evidenced by increased secretion of pro-inflammatory cytokines, pro-coagulatory factors and VEGF. The role of NO in COVID-19 and potential therapeutic strategies. Management includes warming measures, hydration, and cardiovascular support. 2012;36:5715. Data from randomized controlled clinical trials are scarce. 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. Article Front Immunol. Anti-SARS-CoV-2 action of fluvoxamine may be mediated by endothelial nitric oxide synthase. 2020;126:167181. JAMA Netw Open. JAK/STAT pathway is a canonical pathway in driving inflammation. 2021;7:115665. Proc Natl Acad Sci USA. Single-cell transcriptomic atlas of primate cardiopulmonary aging. 2021;24:4036. Hu X, Li J, Fu M, Zhao X, Wang W. The JAK/STAT signaling pathway: from bench to clinic. Would you like email updates of new search results? 2023;17(9):105. doi: 10.1007/s11783-023-1705-1. 2022;9:826218. Pharmacol Rev. Effect of early treatment with fluvoxamine on risk of emergency care and hospitalisation among patients with COVID-19: the TOGETHER randomised, platform clinical trial. Syndecan-1, an indicator of endothelial glycocalyx degradation, predicts outcome of patients admitted to an ICU with COVID-19. 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. Because each symptom can be traced to the autonomic nervous system and its dysfunction, a platform for investigation is clear. Zhang L, Zhou L, Bao L, Liu J, Zhu H, Lv Q, et al. Since atherosclerosis is an important cause for coronary artery disease, it might be of interest to investigate whether COVID-19 can accelerate the development of endothelial dysfunction and new onset atherosclerosis [26]. Kim WY, Kweon OJ, Cha MJ, Baek MS, Choi SH. Endothelial cell number is determined by the balance of cell proliferation and cell death. COVID-19 is characterized by excessive production of inflammatory mediators (IL-1, IL-6, IL-8, TNF-, MCP-1, IP10, RANTES, G-CSF and M-CSF) in a small portion of severe cases due to the severe cytokine storm [60,61,62]. Airway, lung parenchymal, pulmonary vascular, and respiratory neuromuscular disorders all feature in COVID-19. EBioMedicine. Phytother Res. IL-6 trans-signaling induces plasminogen activator inhibitor-1 from vascular endothelial cells in cytokine release syndrome. eLife. Role of traditional chinese medicine in treating severe or critical covid-19: a systematic review of randomized controlled trials and observational studies. 2021;164:6982. BJ9100000005), and Hefei Municipal Development and Reform Commission Emergency Funding for COVID-19 disease. Endothelin-1 is increased in the plasma of patients hospitalised with Covid-19. Handb Clin Neurol. Non-coding RNA. These evidences signify their potential prognostic value to predict severity and mortality of COVID-19 [103, 107]. Statins are prescribed as the first-choice treatment for patients with hypercholesterolemia and coronary artery disease due to their lipid-lowering and pleiotropic anti-inflammatory, antioxidant, anti-thrombotic and immune-modulatory effects. Endothelial cells are not productively infected by SARS-CoV-2. Cytokine storm in COVID-19 can trigger inflammation via the JAK/STAT pathway, which results in increased recruitment of leukocytes/immune cells [146]. 2020;9:1652. Large-scale clinical trials are warranted to evaluate whether the use of SGLT2 inhibitors can reduce the mortality and hospitalizations for heart failure in COVID-19 patients with or without T2DM. MacKenzie MA, Hermus AR, Wollersheim HC, Binkhorst RA, Pieters GF. Hyperpyrexia is an elevation of body temperature above 106.7F (41.5C) due to an abnormally increased hypothalamic-thermoregulatory set. In addition, COVID-19 is an important risk factor for developing acute myocardial infarction [29]. Ebihara T, Matsumoto H, Matsubara T, Togami Y, Nakao S, Matsuura H, et al. Milani GP, Macchi M, Guz-Mark A. Vitamin C in the treatment of COVID-19. 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]. Heat production and dissipation are dependent on a coordinated set of autonomic responses. In addition, mtDNA release also increased vascular reactivity to ET1[94]. COVID-19 is an endothelial disease in which endothelial dysfunction played a major role. NO is one of the most important vasodilatory substances produced by the vascular endothelium with the action of the endothelial NO synthase (eNOS) and several cofactors. Efficacy and tolerability of bevacizumab in patients with severe Covid-19. Despite the observed benefits of HIVC, conflicting results have been reported in severe COVID-19 patients [159]. A recent study has shown that SARS-CoV-2 infection in humanized K18-hACE-2 mice activates the NLRP3 inflammasome, followed by caspase-1 and IL-1 activation[140]. The net effect of SARS-COV-2 infection induced senescence and angiogenesis is potentially dependent on stage of disease. Both SARS-CoV and SARS-CoV-2 utilizes ACE2 and membrane-bound co-factors for virus entry. After virus infection, ensuing cytokine storm occurs in severe COVID-19 patients, particularly the elevated secretion of pro-inflammatory cytokine interleukin 6 (IL-6). Endothelial to mesenchymal transition: a precursor to post-COVID-19 interstitial pulmonary fibrosis and vascular obliteration? Targeting endothelial dysfunction in eight extreme-critically ill patients with COVID-19 using the anti-adrenomedullin antibody adrecizumab (HAM8101). Using force spectroscopy method, a recent study has revealed the binding of glycocalyx with Spike protein, thus precluding S protein/ACE2 interaction. Mental status changes and core temperature distinguish potentially fatal heat stroke from heat exhaustion. A significant proportion of people who test positive for COVID-19 have chemosensory deficits. 2022;13:930673. 2021;15:70417. Direct activation of endothelial cells by SARS-CoV-2 nucleocapsid protein is blocked by simvastatin. Ngele MP, Haubner B, Tanner FC, Ruschitzka F, Flammer AJ. It remains elusive whether COVID-19 patient should continue or initiate statin therapy. Heterogeneous ACE2 expression and endothelial damage was observed in COVID-19 autopsy tissues. 2020;11:605908. Ni L, Wen Z, Hu X, Tang W, Wang H, Zhou L, et al. COVID-19 is associated with several common symptoms in the acute phase that can linger during recovery. N Engl J Med. 2020;314:5862. Clipboard, Search History, and several other advanced features are temporarily unavailable. 2022;52:e13726. Choudhary S, Sharma K, Singh PK. Deaths from . Cells. 2021;10:186. DAgnillo F, Walters KA, Xiao Y, Sheng ZM, Scherler K, Park J, et al. Aging Dis. NO also has an anti-thrombotic action, by preventing leukocyte and platelet adhesion to activated endothelium, thereby inhibiting immunothrombosis and atherosclerotic plaque development [15]. 2022;10:812. de Rooij L, Becker LM, Carmeliet P. A role for the vascular endothelium in post-acute COVID-19? Luca Perico, Ariela Benigni, Giuseppe Remuzzi, Aldo Bonaventura, Alessandra Vecchi, Antonio Abbate, Zoya O. Serebrovska, Elisa Y. Chong, Lei Xi, Rafael Bellotti Azevedo, Bruna Gopp Botelho, Elizabeth Silaid Muxfeldt, Sarah Halawa, Soni S. Pullamsetti, Magdi H. Yacoub, Anglica Arcanjo, Jorgete Logullo, Alexandre Morrot, Toshifumi Matsuyama, Shawn P. Kubli, Tak W. Mak, Acta Pharmacologica Sinica 2021;133:489507. mBio. Health Sci Rep. 2022;5:e762. Joffre J, Rodriguez L, Matthay ZA, Lloyd E, Fields AT, Bainton RJ, et al. J Mol Cell Cardiol. Researchers from the University of Milan, Italy have found a link between thyroid dysfunction and moderate-to-severe COVID-19. It is initially conceived that ACE inhibitors (ACEIs) or Ang-II receptor blockers (ARBs), two widely-used anti-hypertensive drugs targeting the renin-angiotensin system (RAS), could increase the vulnerability to SARS-CoV-2 by upregulating the expression of ACE-2. Potential role of statins in COVID-19. Elevated level of VEGF in senescent ECs and COVID-19 patients are potent trigger of increased angiogenesis in patient tissues, underlying the clinical utility of anti-VEGF treatment for COVID-19 patients [86, 87]. 2021;178:38648. These results suggest that statins can be exploited to treat COVID-19 patients by mitigating endotheliopathy [45, 121].
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