Lei Y, Zhang J, Schiavon CR, He M, Chen L, Shen H, et al. Guzik TJ, Mohiddin SA, Dimarco A, Patel V, Savvatis K, Marelli-Berg FM, et al. Therefore, ACE2 expression may have paradoxical effects, aiding SARS-CoV-2 pathogenicity, yet conversely limiting viral infection [87, 130]. Ikonomidis I, Pavlidis G, Katsimbri P, Lambadiari V, Parissis J, Andreadou I, et al. There are multiple lines of evidences suggesting the involvement of endothelial dysfunction in COVID-19 [45]. 2022;13:926189. Pathogenesis and Transmission of COVID-19. 2022;19:149. 2021;13:23424. 2021;7:9. Choudhary S, Sharma K, Singh PK. 4 and 5) [101]. Suzuki K, Okada H, Tomita H, Sumi K, Kakino Y, Yasuda R, et al. SARS-CoV-2 targets the pulmonary system, as well as the extrapulmonary system [2]. First, thermoregulatory dysfunction is a well-known sequela after spinal cord injury, due to disruption of neurologic signals to and from the hypothalamic temperature regulation center. It is appreciated that SARS-CoV-2 infection can trigger systemic vascular injury through binding to ACE2. 2022. https://doi.org/10.1164/rccm.202107-1774OC. These findings suggest that fluvoxamine can be repurposed as novel anti-COVID-19 drugs although further studies are warranted to assess the therapeutic potential of fluvoxamine in patients [151]. 2022;96:3441. Tomasa-Irriguible TM, Bielsa-Berrocal L. COVID-19: Up to 82% critically ill patients had low vitamin C values. 2021;19:5. : Experimental results and a cautionary note on challenges in translational research. Endothelial contribution to COVID-19: an update on mechanisms and therapeutic implications. 2020;145:111694. 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]. Front Med. Vollenberg R, Tepasse PR, Ochs K, Floer M, Strauss M, Rennebaum F, et al. 2022;9:826218. Eur Heart J. 2021;27:151. SARS-CoV-2 and COVID-19: The most important research questions. sharing sensitive information, make sure youre on a federal Ma Z, Yang KY, Huang Y, Lui KO. Wu D, Lee TH, Huang RT, D Guzy R, Schoettler N, Adegunsoye A, et al. 2021;8:687783. SARS-CoV-2 spike protein S1-mediated endothelial injury and pro-inflammatory state is amplified by dihydrotestosterone and prevented by mineralocorticoid antagonism. Med Intensiv. Therefore, maintaining the integrity of glycocalyx offers new strategies to combat COVID-19 associated endothelial dysfunction [114]. Targeting inflammation and cytokine storm in COVID-19. Postgrad Med. A recent study has shown that increased levels of cellular senescence-associated markers, including PAI-1, p21 and sirtuin-1 in patient serum as well as lung ECs [89]. Horby P, Lim WS, Emberson JR, Mafham M, Bell JL, Linsell L, et al. Hypothermia, defined as a core temperature of <35.0C, may present with shivering, respiratory depression, cardiac dysrhythmias, impaired mental function, mydriasis, hypotension, and muscle dysfunction, which can progress to cardiac arrest or coma. 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. 2020;116:1097100. Relationship between endothelial and angiogenesis biomarkers envisage mortality in a prospective cohort of COVID-19 patients requiring respiratory support. Raghavan S, Kenchappa DB, Leo MD. Virus-induced senescence is a pathogenic trigger of endothelial dysfunction. 2017;12:e0186116. 2021;10:e69314. 2021YFC2500500), National Natural Science Foundation of China (Grant No. Employing mechanical ventilation techniques on venovenous extracorporeal membrane oxygenation (VV ECMO . 2021;12:609470. During the course of COVID-19 pneumonia, thyrotoxicosis may be caused secondary to graves thyroiditis or subacute inflammatory thyroiditis. CAS Ilonzo N, Judelson D, Al-Jundi W, Etkin Y, OBanion LA, Rivera A, et al. Recently, miR-98-5p was identified as a negative regulator of TMPRSS2 gene transcription in human lung and umbilical vein ECs [98]. These include tachycardia, shortness of breath, fatigue and post-exercise exhaustion. Deaths from hypothermia are twice as frequent as deaths from hyperthermia. Hu B, Huang S, Yin L. The cytokine storm and COVID-19. Disclaimer. CD209L/L-SIGN and CD209/DC-SIGN act as receptors for SARS-CoV-2. In-hospital use of statins is associated with a reduced risk of mortality among individuals with COVID-19. 2020;383:225573. Xia G, Qin B, Ma C, Zhu Y, Zheng Q. High-dose vitamin C ameliorates cardiac injury in COVID-19 pandemic: a retrospective cohort study. 2020;10:1171. Gupta A, Madhavan MV, Sehgal K, Nair N, Mahajan S, Sehrawat TS, et al. Maldonado F, Morales D, Daz-Papapietro C, Valds C, Fernandez C, Valls N, et al. Also, CD209L/L-SIGN was identified as another receptor for mediating SARS-CoV-2 entry into human cells which can also interacts with ACE2 to facilitate SARS-CoV-2 entry [21]. These findings suggest that spike protein interactions with ECs contribute to inflammation, thrombosis, and the severity of COVID-19 and could offer novel mechanistic insights into SARS-CoV-2 induced vascular leakage and the development of targeted therapies [59]. 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]. Cell Res. 2021;185:106469. However, the underlying cellular and molecular mechanisms driving this condition are . 2022;43:217390. Medicine (Baltimore). Further, removal of the N-glycosylation site at N92 of L-SIGN enhances the binding of S-RBD with L-SIGN [21]. Article Cardiovasc Res. JAMA Netw Open. 8600 Rockville Pike 2) [2, 16]. 2. Dupont A, Rauch A, Staessens S, Moussa M, Rosa M, Corseaux D, et al. 5. Thermoregulation is a vital function of the autonomic nervous system in response to cold and heat stress. Basta G. Direct or indirect endothelial damage? Mitochondrial DNA and TLR9 activation contribute to SARS-CoV-2-induced endothelial cell damage. Hyperpyrexia is an elevation of body temperature above 106.7F (41.5C) due to an abnormally increased hypothalamic-thermoregulatory set. Researchers from the University of Milan, Italy have found a link between thyroid dysfunction and moderate-to-severe COVID-19. Henry BM, de Oliveira MHS, Cheruiyot I, Benoit JL, Cooper DS, Lippi G, et al. Endothelial dysfunction, inflammation, and oxidative stress in COVID-19-mechanisms and therapeutic targets. Signal Transduct Target Ther. Ni L, Wen Z, Hu X, Tang W, Wang H, Zhou L, et al. Huang Q, Wu X, Zheng X, Luo S, Xu S, Weng J. Physiological functions of the endothelium include fine control of vascular tone, tissue hemostasis, barrier integrity, inflammation, oxidative stress, vascular permeability, and structural and functional integrity [4]. Six I, Guillaume N, Jacob V, Mentaverri R, Kamel S, Boullier A, et al. SARS-CoV-2 can cross the blood brain barrier without affecting the expression of tight junctions (claudin5, ZO-1 and occludin) [41]. Wenzel J, Lampe J, Mller-Fielitz H, Schuster R, Zille M, Mller K, et al. Heparin prevents in vitro glycocalyx shedding induced by plasma from COVID-19 patients. COVID-19 and thermoregulation-related problems: Practical recommendations Description An international research team organized by the Global Heat Health Information Network prepared an inventory of the specific concerns about heat related illness and coronavirus transmission and began to address the issues. Prevention of skin lesions caused by the use of protective face masks by an innovative gelatin-based hydrogel patch: Design and in vitro studies. Article 3). J Infect Dis. Ding Y, Zhou Y, Ling P, Feng X, Luo S, Zheng X, et al. 2020;395:14178. The infected cell releases danger signals leading to multiple aspects of endothelial dysfunction, which finally leads to impaired vascular activity and multi-organ injury. Endothelial dysfunction in COVID-19: Current findings and therapeutic implications. Noris M, Benigni A, Remuzzi G. The case of complement activation in COVID-19 multiorgan impact. Therefore, IL-6 trans-signaling represents the mechanistic link between the coagulopathy/endotheliopathy and COVID-19 associated liver injury [35]. The American-European Consensus Conference definition of the acute respiratory distress syndrome is dead, long live positive end-expiratory pressure! A recent randomized clinical trial has shown that heparin treatment was not significantly associated with reduction of primary outcome, but associated with decreased odds of death at 4 weeks [129]. Tetlow S, Segiet-Swiecicka A, OSullivan R, OHalloran S, Kalb K, Brathwaite-Shirley C, et al. A recent review has proposed the detailed mechanism of SARS-CoV-2 induced mtROS production and the consequence of it, including cardio-pulmonary injury associated with COVID-19. J Inflamm Res. J Hepatol. Ice water immersion has been shown to be superior to alternative cooling measures. EBioMedicine. Top manufacturers . The polypharmacological profile of metformin makes it a promising candidate drug to be repurposed for controlling inflammation tsunami in diabetic COVID-19 patients [124]. Evidently, based on the cytokine storm in severe or critically ill COVID-19 patients, targeted inhibition of pro-inflammatory cytokines, such as IL-1, IL-6 and downstream signal transduction pathways appears to be important avenues [93]. Signal Transduct Target Ther. Rotoli BM, Barilli A, Visigalli R, Ferrari F, DallAsta V. Endothelial cell activation by SARS-CoV-2 Spike S1 protein: a crosstalk between endothelium and innate immune cells. 3). Molecular underpinnings of metabolic alterations caused by SARS-CoV-2 infection warrants further studies; Lastly, considering the evolving mutations of SARS-CoV-2 (such as Delta variant and Omicron variant), effect and mechanism of these variants in viral entry and endothelial functionality warrant further studies. 2022;145:15035. The authors declare no competing interests. Am J Respir Crit Care Med. Besides directly infected by SARS-CoV-2, the ECs also undergo injury by systemic inflammation caused by over-activation of innate immune response, referring to cytokine storm [91, 92]. 2021;24:152233. 7). Endothelial dysfunction-induced endotheliitis/endothelialitis/endotheliopathy following SARS-CoV-2 infection arises from a plethora of physiopathological mechanisms, including both direct mechanism of virus infection or indirect mechanisms such as paracrine effects of infected cells [2, 68]. 1) [14]. SGLT2 inhibitors can reduce the composite endpoint of cardiovascular death and HF hospitalizations in heart failure patients either with reduced ejection fraction or preserved ejection fraction. Lopes-Paciencia S, Saint-Germain E, Rowell MC, Ruiz AF, Kalegari P, Ferbeyre G. The senescence-associated secretory phenotype and its regulation. Since the outbreak of COVID-19 in early 2020, emerging evidence has demonstrated endothelial dysfunction as the unifying and central mechanism of COVID-19 [6]. 2021;95:e0079421. In a randomized clinical trial, L-arginine add-on therapy significantly reduces the length of hospitalization in severe COVID-19 patients and reduces the need of respiratory support, with no serious adverse events [147]. Targeting endothelial dysfunction in eight extreme-critically ill patients with COVID-19 using the anti-adrenomedullin antibody adrecizumab (HAM8101). 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. TCM has a well-documented safety profile in protecting against COVID-19 on the basis of standard care. EBioMedicine. Nutrients. Yuen KS, Ye ZW, Fung SY, Chan CP, Jin DY. Role of angiotensin-converting enzyme 2 (ACE2) in COVID-19. A meta-analysis revealed the favorable effect of statins in COVID-19 patients [118]. A new study by investigators from the Smidt Heart Institute at Cedars-Sinai suggests long COVID-19 might be caused by a dysfunction of . A systematic review and case report analysis. It is reported that COVID-19-patients had higher number of CECs than COVID-19-free subjects. Varga Z, Flammer AJ, Steiger P, Haberecker M, Andermatt R, Zinkernagel AS, et al. A recent study has shown that markers associated with endothelial inflammation and injury pathway (IL-6, TNF-, ICAM-1 and caspase-1) were observed in the lung tissues from COVID-19 patients compared with H1N1 subtype 2009 and control cases [63]. Slider with three articles shown per slide. Severe COVID-19 is a microvascular disease. Theranostics. Food Chem Toxicol. the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Oxid Med Cell Longev. Mortality risk among patients with COVID-19 prescribed selective serotonin reuptake inhibitor antidepressants. RNA-sequencing data further revealed the increased expression of markers of endothelial activation such as RELB (p50 subunit) and TNF- [65]. Front Med. Int J Obes (2005). Sulodexide significantly improves endothelial dysfunction and alleviates chest pain and palpitations in patients with long-COVID-19: Insights From TUN-EndCOV study. Sci Transl Med. Biomedicines. However, several JAK/STAT inhibitors such as ruxolitinib, tofacitinib and baricitinib can suppress cytokine signaling cascade. 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]. This study was supported by grants from National Key R&D Program of China (Grant No. Front Environ Sci Eng. QJM. HIVC also protect against severe COVID-19 by decreasing the rates of mechanical ventilation and cardiac arrest in hospitalized severe patients [156]. Cell. This study provides additional clinical evidence supporting continuation of metformin use in COVID-19 patients with pre-existing T2DM by paying close attention to kidney function and acidosis [126]. Cell Mol Life Sci. 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 . Google Scholar. EndoMT can be induced by cytokine mixture in cultured endothelial cells, for example, the combination of TNF- and IL-1, IL-1 and TGF1, etc. 2021;13:1172. Effect of early treatment with fluvoxamine on risk of emergency care and hospitalisation among patients with COVID-19: the TOGETHER randomised, platform clinical trial. 2021;53:18695. Colchicine is an anti-inflammatory drug traditionally used in gout and familial Mediterranean fever [143, 144]. The burst of ROS after SARS-CoV-2 infection will elicit long-term deleterious effects on endothelial cells, including decreased eNOS expression and NO bioavailability as well as flow-mediated vasodilation in COVID-19 patients. 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]. 2022;75:103812. Zhang L, Zhou L, Bao L, Liu J, Zhu H, Lv Q, et al. The effect of glucocorticoids on COVID-19 might be multifactorial, and their endothelium-stabilizing properties by direct activation of endothelial glucocorticoid receptors to block production of IL-6 and VEGF might be the main operating mechanisms [19]. Ambrosino P, Calcaterra IL, Mosella M, Formisano R, DAnna SE, Bachetti T, et al. SARS-CoV-2 Spike triggers barrier dysfunction and vascular leak via integrins and TGF- signaling. Failure of neural thermoregulatory mechanisms or exposure to extreme or sustained temperatures that overwhelm the body's thermoregulatory capacity can also result in potentially life-threatening departures from normothermia. Front Pharmacol. Increased complement activation is a distinctive feature of severe SARS-CoV-2 infection. Arch Med Res. Fiorentino G, Coppola A, Izzo R, Annunziata A, Bernardo M, Lombardi A, et al. In addition, the release of inflammatory cytokines after severe SARS-CoV-2 infection leads to cytokine storm, tight junction barrier disruption, pulmonary hypertension, and lung fibrosis [24]. The spatio-temporal release of VEGF-A and its effects on endothelial proliferation, migration and capillary-like tube formation warrant further study. Severe COVID-19-induced cytokine storm (such as IL-6, IL-1, TNF-, MCP-1, etc) is a good predictor ofthe severity of COVID-19, which also aggravates multi-organ injury by propagating the vicious cycle of ECs damage, inflammation and thrombosis [93]. 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. Vasculopathy in COVID-19. 2023 Jan;18(1):36-41. doi: 10.2185/jrm.2022-016. Front Med. Pharmacological inhibition of senescence or SASP can reverse endothelial inflammation and leukocyte adhesion. Cardiovasc Res. ACE2 can also undergo shedding and the soluble form of ACE2 (sACE2) can be released into circulating blood. Careers. Int J Infect Dis. A significant proportion of people who test positive for COVID-19 have chemosensory deficits. Antiviral therapies and effective vaccination reduce viral load and could potentially offer endothelial protection in perivascular spaces [19]. Eur J Intern Med. 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. Endothelin-1 is increased in the plasma of patients hospitalised with Covid-19. This work was also supported by Program for Innovative Research Team of The First Affiliated Hospital of USTC (CXGG02), Anhui Provincial Key Research and Development Program (Grant No. Kumar N, Zuo Y, Yalavarthi S, Hunker KL, Knight JS, Kanthi Y, et al. Several histopathological evidence has supported direct viral infection of endothelial cells, for example, electron microscopy of kidney tissues shows the existence of endotheliitis and viral particles in ECs [52]. Thermoregulatory dysfunction is defined as significant loss of a person's capacity to control body temperature, and the medical conditions which result in the person's health and bodily function being seriously affected when exposed to extremes of environmental temperatures. Sur S, Steele R, Isbell TS, Ray R, Ray RB. These targets are directed at improving oxidative stress, endothelial inflammation/inflammasome, senescence, fibrosis, cell death, thrombosis, coagulopathy, angiogenesis, EndoMT and immunity mechanisms. Bethesda, MD 20894, Web Policies These effects were blocked by soluble glycoprotein 130, ruxolitinib, and STAT1/3 depletion. Federal government websites often end in .gov or .mil. These data agree with recent report of the clinical benefits of statin therapy in lowering the risk of mortality of COVID-19 [119]. Endothelial cells are not productively infected by SARS-CoV-2. These evidences suggest that inhibition of complement pathway could be an effective strategy to manage endothelial injury/endotheliitis accompanying COVID-19 [97]. Aging Dis. The disrupted glycocalyx structure leads to hyperinflammatory response and oxidative stress, which leads to increased susceptibility to SARS-CoV-2 infection [67]. The decrease of NO bioavailability occurs partially because of a decrease in eNOS-derived NO production and enormous production of reactive oxygen species (ROS), which inactivates eNOS and causes eNOS uncoupling. Qian Y, Lei T, Patel PS, Lee CH, Monaghan-Nichols P, Xin HB, et al. 2022;119:31925. Extrapulmonary manifestations of COVID-19. It remains elusive whether COVID-19 patient should continue or initiate statin therapy. SARS-CoV-2 infection of human brain microvascular endothelial cells leads to inflammatory activation through NF-B non-canonical pathway and mitochondrial remodeling. Kondo Y, Larabee JL, Gao L, Shi H, Shao B, Hoover CM, et al. Pine AB, Meizlish ML, Goshua G, Chang CH, Zhang H, Bishai J, et al. Potential role of statins in COVID-19. Han T, Ma S, Sun C, Zhang H, Qu G, Chen Y, et al. 2022;55:57. Won T, Wood MK, Hughes DM, Talor MV, Ma Z, Schneider J, et al. Liu Y, Zhang HG. Potje SR, Costa TJ, Fraga-Silva TFC, Martins RB, Benatti MN, Almado CEL, et al. In addition, COVID-19 is an important risk factor for developing acute myocardial infarction [29].
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