volume44,pages 695709 (2023)Cite this article. 2022;9:866113. Thermoregulatory dysfunction energy subsidy | energy.gov.au Epub 2023 Jan 6. Effect of anakinra on mortality in patients with COVID-19: a systematic review and patient-level meta-analysis. Theranostics. 2021;133:489507. 2022: 1-10. Provided by the Springer Nature SharedIt content-sharing initiative, Acta Pharmacologica Sinica (Acta Pharmacol Sin) Pan R, Xie M, Chen M, Zhang Y, Ma J, Zhou J. The site is secure. Adv Physiol Educ. Pulm Circ. Combinatorial treatment of human ECs with TNF- and IFN- increased the expression of ACE2, the receptor mediating viral entry via JAK/STAT1 pathway [13]. Fardman A, Zahger D, Orvin K, Oren D, Kofman N, Mohsen J, et al. It has been reported that injury to the endothelial glycocalyx and the release of syndecan-1 (SDC-1) was observed in severe COVID-19 patients [69, 70]. Prevalence of Chemosensory Dysfunction in COVID-19 Patients: A In vivo, SARS-CoV-2-infected K18 mice develop severe COVID-19 and endothelial dysfunction in pulmonary vessels suggested by VCAM-1 and ICAM-1 upregulation and VE-cadherin downregulation [78]. Aging Dis. Fajgenbaum DC, June CH. 2020;73:123140. 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]. The most common cardiovascular complications of COVID-19 include arrhythmia, cardiac injury (evidenced by elevated troponin I, creatine kinase, NT-proBNP levels), coagulation (evidenced by elevated level of D-dimer), fulminant myocarditis, heart failure and new-onset atherosclerosis [26]. Similar effects were observed in ECs infected with SARS-CoV-2 spike pseudovirions (SCV-2-S) [55]. Zhang P, Zhu L, Cai J, Lei F, Qin JJ, Xie J, et al. Endothelial to mesenchymal transition: a precursor to post-COVID-19 interstitial pulmonary fibrosis and vascular obliteration? Redox Biol. Electron microscopy also show coronaviruses and vesicles containing virion particles in venous ECs [53] as well as LSECs from liver autopsy samples from COVID-19 patients [33]. Internet Explorer). In addition, heparan sulphate, as the major component in the glycocalyx, can also regenerate glycocalyx and promote the effective restoration of homeostatic EC gap junction [111]. Front Med. Lee S, Yu Y, Trimpert J, Benthani F, Mairhofer M, Richter-Pechanska P, et al. HIVC improves myocardial injury via decreasing biomarkers associated with inflammation in critically ill COVID-19 patients [155]. Brain Pathol (Zur, Switz). Clinical and pathological investigation of patients with severe COVID-19. Reis G, Dos Santos Moreira-Silva EA, Silva DCM, Thabane L, Milagres AC, Ferreira TS, et al. Metformin represents the first-line therapy for T2DM [123]. 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. In-hospital use of statins is associated with a reduced risk of mortality among individuals with COVID-19. 2020;40:24047. 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 ). Employing mechanical ventilation techniques on venovenous extracorporeal membrane oxygenation (VV ECMO . Potential mechanisms of coronavirus disease 2019 (COVID-19)-induced olfactory dysfunction. A recent study has demonstrated that SARS-CoV-2 infection increased superoxide anion production, and mitochondrial DNA (mtDNA) release, leading to the activation of TLR9 and NF-B, which orchestrates the expression of inflammatory genes[94]. Cardiovasc Res. TACT on Twitter: ""Persisting pulmonary dysfunction in pediatric post Circulation. 2021;13:23424. Cellular senescence was also associated with endothelial inflammation (augmented expression of ICAM-1 and VCAM-1), which is essential for promoting leukocyte adhesion to activated endothelium. DAgnillo F, Walters KA, Xiao Y, Sheng ZM, Scherler K, Park J, et al. Anakinra for severe forms of COVID-19: a cohort study. Amraei R, Rahimi N. COVID-19, Renin-Angiotensin system and endothelial dysfunction. Endothelial dysfunction in COVID-19: an overview of evidence 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. (i) COVID-19 directly affects sustentacular (SUS) cells through interactions with the ACE2 receptor, thereby leading to abnormal transmission of odor molecules. This shows that olfactory and especially gustatory disorders have to be seen as important chronic symptoms post-COVID-19. 2021;6:266. 2022;115:7783. 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]. QJM. NO also has an anti-thrombotic action, by preventing leukocyte and platelet adhesion to activated endothelium, thereby inhibiting immunothrombosis and atherosclerotic plaque development [15]. In addition, mtDNA release also increased vascular reactivity to ET1[94]. Erectile Dysfunction Drugs Market Market Projection and - MarketWatch 2020;98:31422. However, the pathophysiology of acute and post-acute manifestations of COVID-19 (long COVID-19) is understudied. However, conclusions need to be analyzed with caution due to small sample size [165]. SGLT2 inhibitors are rising stars in cardiovascular and diabetic arena due to prominent cardiorenal benefits in several large-scale clinical trials [127]. Further outstanding questions and research directions in the realm of endothelial dysfunction and COVID-19 include the following: The development of assays of assessing endothelial function in long COVID-19 patients and convalescents, such as brachial artery flow-mediated dilation (FMD) and arterial stiffness [carotid-femoral pulse wave velocity (cfPWV)]; This aspect is important considering the recent observation showing the decreased FMD in patients with COVID-19 stemming from expression of inflammatory cytokines/chemokines [176]; Cellular and animal models of evaluating endothelial dysfunction in COVID-19 to accelerate drug discovery; The therapeutic potential of specialized pro-resolving lipid mediators, such as resolvin D1, resolvin E1, aspirin-triggered resolvin D1 in resolving cytokine storm induced inflammatory responses can be pursued; The identification of alternative receptors for SARS-CoV-2 infection into different vascular beds beyond known ones (such as ACE2, AXL and L-SIGN) remain to be identified; Drug repurposing or high-throughput drug screening to identify new drugs targeting endothelial dysfunction in COVID-19; The role of epigenetic modification arising from DNA methylation and histone modification and long-lasting epigenetic memory effects caused by SARS-CoV2 infection in long COVID (postacute COVID-19 syndrome) remain to be evaluated [7]; Metabolic disturbance has been shown to be associated with the pathogenesis of COVID-19 [177]. SARS-CoV-2 infection alters the balance of endothelial protective molecules and endothelial damaging molecules, leading to endothelial dysfunction. Huang Q, Wu X, Zheng X, Luo S, Xu S, Weng J. Matarese A, Gambardella J, Sardu C, Santulli G. miR-98 regulates TMPRSS2 expression in human endothelial cells: key implications for COVID-19. Increased plasma level of soluble P-selectin in non-hospitalized COVID-19 convalescent donors. Life Sci. Acute myocardial infarction and myocarditis following COVID-19 vaccination. Kandhaya-Pillai R, Yang X, Tchkonia T, Martin GM, Kirkland JL, Oshima J. TNF-/IFN- synergy amplifies senescence-associated inflammation and SARS-CoV-2 receptor expression via hyper-activated JAK/STAT1. Forensic Sci Med Pathol. Management requires the immediate reduction of core temperature. This site needs JavaScript to work properly. These drugs include lipid-lowering drugs, anti-hypertensive drugs, anti-diabetic drugs, anti-VEGF agents, anti-coagulatory drugs, antioxidants, anti-inflammatory drugs and others. ACE2 can also undergo shedding and the soluble form of ACE2 (sACE2) can be released into circulating blood. IL-6 directly impacts vascular ECs by promoting the production of numerous cytokines/chemokines/adhesion molecules essential for promoting leukocyte adhesion, vascular leakage and activating the coagulation cascade [136]. The relationship between mechanisms and biomarkers of endothelial dysfunction in COVID-19 is provided in Fig. ICU admission levels of endothelial biomarkers as predictors of mortality in critically Ill COVID-19 patients. official website and that any information you provide is encrypted Introduction Ice water immersion has been shown to be superior to alternative cooling measures. Circulating markers of angiogenesis and endotheliopathy in COVID-19. [132] and the expert recommendations from the professional cardiovascular societies, supporting that ACEIs and ARBs does not alter SARS-CoV-2 infection and should not be discontinued in COVID-19 patients [133]. PLoS One. Abraham GR, Kuc RE, Althage M, Greasley PJ, Ambery P, Maguire JJ, et al. The protective role of ACE2 agonism in suppressing angiogenesis and maintaining endothelial integrity in COVID-19 warrant further investigation [19]. Effects of Shuanghuanglian oral liquids on patients with COVID-19: a randomized, open-label, parallel-controlled, multicenter clinical trial. Milani GP, Macchi M, Guz-Mark A. Vitamin C in the treatment of COVID-19. In addition to the spike protein, nucleocapsid protein of SARS-CoV-2 can also promotes endothelial activation via TLR2/NF-B and MAPK signaling pathways. 2020;26:101732. Choudhary S, Sharma K, Singh PK. 2021;12:653110. However, the underlying cellular and molecular mechanisms driving this condition are . 2020;46:20812. EClinicalMedicine. 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. Glycocalyx protein component can be degraded by degrading enzyme such as heparinase. Smell and Taste Dysfunction in Patients With COVID-19: A Systematic Acta Pharmacol Sin 44, 695709 (2023). Google Scholar. Cardiovasc Res. 2020;314:5862. . 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]. 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]. PubMed Central Postgrad Med. 2023 Mar 31;102(13):e33345. Torices S, Motta C, da Rosa B, Marcos A, Alvarez-Rosa L, Siqueira M, et al. Study implicates diaphragm dysfunction as a potential cause for Yang RC, Huang K, Zhang HP, Li L, Zhang YF, Tan C, et al. Horby P, Lim WS, Emberson JR, Mafham M, Bell JL, Linsell L, et al. Eur J Intern Med. L-arginine improves endothelial dysfunction by being the substrate of NO generation in endothelial cells. The polypharmacological profile of metformin makes it a promising candidate drug to be repurposed for controlling inflammation tsunami in diabetic COVID-19 patients [124]. Tong M, Jiang Y, Xia D, Xiong Y, Zheng Q, Chen F, et al. Recent studied have shown that colchicine is able to reduce the length of stay in hospitalized COVID-19 patients with the possible mechanism of inhibition of NLRP3 inflammasome and resultant IL-1 production [143, 144]. An official website of the United States government. Fiorentino G, Coppola A, Izzo R, Annunziata A, Bernardo M, Lombardi A, et al. 2012;36:5715. Kim WY, Kweon OJ, Cha MJ, Baek MS, Choi SH. Unraveling the role of liver sinusoidal endothelial cells in COVID-19 liver injury. Thermoregulatory disorders and illness related to heat and - PubMed Cell Biosci. Infection with various types of viruses, including SARS-CoV-2, can trigger endothelial senescence. Thus, the endothelium is regarded as the Achilles heel in COVID-19 patients [8]. Hu B, Huang S, Yin L. The cytokine storm and COVID-19. Coagulation abnormalities and thrombosis in patients with COVID-19 2020;18:23919. 2022;140:22235. 2021;10:e69314. MacKenzie MA, Hermus AR, Wollersheim HC, Binkhorst RA, Pieters GF. Crit Care (Lond, Engl). J Mol Cell Cardiol. Li S, Jiang L, Li X, Lin F, Wang Y, Li B, et al. Circulation. Google Scholar. Injury to the endothelial glycocalyx in critically Ill patients with COVID-19. mBio. J Hepatol. This study highlights the crucial role of IL-6 trans-signaling in endothelial dysfunction/endotheliopathy in COVID-19 [137]. Anyone you share the following link with will be able to read this content: Sorry, a shareable link is not currently available for this article. It has been increasingly appreciated that COVID-19 is not only an infectious disease involving the lung; but also, a vascular disease affecting extrapulmonary organs [174]. ACE2 is described as the first identified receptor responsible for the entry for SARS-CoV-2 into host cells including ECs [46]. The therapeutic potential of senolytics in COVID-19 patients warrants studies from clinical trials. Mitochondrial dysfunction usually occurs after viral infection, thereby exacerbating tissue damage. Impact of sodium glucose cotransporter 2 (SGLT2) inhibitors on atherosclerosis: from pharmacology to pre-clinical and clinical therapeutics. Extrapulmonary manifestations of COVID-19. CAS PEEP in COVID-19 Patients: A Retrospective Study on RV Dysfunction The net consequence is the extravasation of inflammatory and immune cell infiltrations [74]. COVID-19 and the cardiovascular system: implications for risk assessment, diagnosis, and treatment options. Another recent study has demonstrated that, SARS-CoV-2 infection in human brain microvascular ECs increased the secretion of angiogenic factors and altered mitochondrial dynamics, such as increased the expression of mitofusin-2 (a protein involved in a maintenance of an appropriate mitochondrial architecture, metabolism and signaling) and fostered the formation of mitochondrial networks [65]. 2022. https://doi.org/10.1164/rccm.202107-1774OC. In this regard, miR-24-3p has recently been identified as an essential regulator of Neuropilin-1 gene transcription, thereby maintaining barrier integrity via suppressing VEGF-induced endothelial leakage in human brain ECs [99]. 2021;96:256175. The disrupted glycocalyx structure leads to hyperinflammatory response and oxidative stress, which leads to increased susceptibility to SARS-CoV-2 infection [67]. PMC Qin H, Zhao A. Mesenchymal stem cell therapy for acute respiratory distress syndrome: from basic to clinics. Antiviral therapies and effective vaccination reduce viral load and could potentially offer endothelial protection in perivascular spaces [19]. Toscano O, Cosentino N, Campodonico J, Bartorelli AL, Marenzi G. Acute myocardial infarction during the COVID-19 pandemic: an update on clinical characteristics and outcomes. Vitamin C consumption significantly reduces mortality risk with COVID-19 patients [157]. Satarker S, Tom AA, Shaji RA, Alosious A, Luvis M, Nampoothiri M. JAK-STAT pathway inhibition and their implications in COVID-19 therapy.
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