Neurological implications of COVID-19: role of redox imbalance and mitochondrial dysfunction. Of translational significance, COVID-19 patients derived serum also increased mtDNA release in ECs, compared to control subjects. 2021;142:106946. 2021;290:43743. Suo-wen Xu or Jian-ping Weng. CAS COVID-19 is associated with several common symptoms in the acute phase that can linger during recovery. SARS-CoV-2 mediated endothelial dysfunction: the potential role of chronic oxidative stress. Resistin is peptide hormone derived from adipose tissue which is associated with endothelial injury and inflammatory response. 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. Bookshelf In addition, the levels of these endothelial markers are elevated in intensive care units (ICU) non-survivors compared to survivors. Endothelial dysfunction is generally defined as decreased NO bioavailability and an increase in vasoconstrictory substances (such as endothelin-1 (ET1), angiotensin II (AngII) and many others). The glycocalyx consists of highly sulfated proteoglycans with glycosaminoglycan side chains. 2020;126:167181. 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. Ebihara T, Matsumoto H, Matsubara T, Togami Y, Nakao S, Matsuura H, et al. Papadopoulos KI, Sutheesophon W, Aw TC. Torices S, Motta C, da Rosa B, Marcos A, Alvarez-Rosa L, Siqueira M, et al. 2020;116:1097100. Furthermore, spike protein S1 receptor-binding domain (S1-RBD) infection in mouse brain microvascular ECs induced the degradation of endothelial junctional proteins (VE-Cadherin, junctional adhesion molecule-A, Connexin-43 and PECAM-1), thereby impaired endothelial barrier function and caused vascular leakage and endotheliitis in COVID-19 patients [57, 58]. Intern Emerg Med. A new study by investigators from the Smidt Heart Institute at Cedars-Sinai suggests long COVID-19 might be caused by a dysfunction of . EBioMedicine. 3). The endothelium and COVID-19: an increasingly clear link brief title: endotheliopathy in COVID-19. SARS-CoV-2 Spike triggers barrier dysfunction and vascular leak via integrins and TGF- signaling. 2021;16:e0253524. Sur S, Steele R, Isbell TS, Ray R, Ray RB. Long COVID Patients Respond Differently to COVID Vaccines - WebMD 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. J Hepatol. 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]. SARS-CoV-2 causes ACE/ACE2 balance disruption and RAAS activation, which leads ultimately to COVID-19 progression, especially in patients with comorbidities, such as hypertension, diabetes mellitus, and cardiovascular disease. 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. Eur J Clin Invest. ACE2 is highly expressed in renal tissues, the injury of which leads to proteinuria, hematuria and abnormal renal radiography [38]. Henry BM, de Oliveira MHS, Cheruiyot I, Benoit JL, Cooper DS, Lippi G, et al. 2021;53:111623. The fight against coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 infection is still raging. The elevated VEGF-A level further promotes endothelial leakage and inflammatory cell infiltration [19]. Deaths from hypothermia are twice as frequent as deaths from hyperthermia. Dexamethasone may improve severe COVID-19 via ameliorating endothelial injury and inflammation: A preliminary pilot study. Endothelial dysfunction in COVID-19: an overview of evidence Analysis of ACE2 expression in autopsy tissues indicates that high expression of ACE2, transmembrane protease serine 2 (TMPRSS2) and associated endotheliitis in capillaries but less in arterioles/venules from COVID-19 patients, compared with COVID-19-free subjects. 4 and 5) [101]. Circulatory exosomes from COVID-19 patients trigger NLRP3 inflammasome in endothelial cells. Results of the first interim analysis. (i) COVID-19 directly affects sustentacular (SUS) cells through interactions with the ACE2 receptor, thereby leading to abnormal transmission of odor molecules. Online ahead of print. Matarese A, Gambardella J, Sardu C, Santulli G. miR-98 regulates TMPRSS2 expression in human endothelial cells: key implications for COVID-19. Endothelial damage in acute respiratory distress syndrome. 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]. It remains to be investigated whether other mechanisms that are more closely related to COVID-19, such as long non-coding RNA, circular RNA, RNA methylation, microbiota and metabolites, are involved in triggering endothelial dysfunction following SARS-COV-2 infection. 2020;2:e393e400. Arterial stiffness in acute COVID-19 and potential associations with clinical outcome. Amraei R, Yin W, Napoleon MA, Suder EL, Berrigan J, Zhao Q, et al. Pathway enrichment analysis revealed that SARS-CoV-2 infection upregulates expression of genes enriched in signaling pathways relevant to inflammatory response (such as NF-kappa B signaling pathway, TLR signaling pathway, NLRP3 pathway, NOD-like receptor signaling pathway and cytokinecytokine receptor interaction) [75]. Choudhary S, Sharma K, Singh PK. 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]. Ma L, Sahu SK, Cano M, Kuppuswamy V, Bajwa J, McPhatter J, et al. Resistin associated with cytokines and endothelial cell adhesion molecules is related to worse outcome in COVID-19. FOIA 2021;15:70417. COVID-19 and thermoregulation-related problems: Practical Effect of early treatment with fluvoxamine on risk of emergency care and hospitalisation among patients with COVID-19: the TOGETHER randomised, platform clinical trial. Evaluation of endothelial dysfunction in COVID-19 with flow-mediated dilatation. Jover E, Matilla L, Garaikoetxea M, Fernndez-Celis A, Muntendam P, Jaisser F, et al. Front Immunol. Okada H, Yoshida S, Hara A, Ogura S, Tomita H. Vascular endothelial injury exacerbates coronavirus disease 2019: The role of endothelial glycocalyx protection. Ackermann M, Verleden SE, Kuehnel M, Haverich A, Welte T, Laenger F, et al. After that, STATs translocate into cell nucleus to orchestrate the expression of inflammatory cytokines, further instigating the cytokine storm feedback loop. Thermoregulation is a vital function of the autonomic nervous system in response to cold and heat stress. 2022;10:e42e51. 82070464, 81941022, 81530025) and Strategic Priority Research Program of Chinese Academy of Sciences (Grant No. Front Immunol. Costa TJ, Potje SR, Fraga-Silva TFC, da Silva-Neto JA, Barros PR, Rodrigues D, et al. Google Scholar. 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]. 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. 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. Pharmacopsychiatry. COVID-19 and thermoregulation-related problems: Practical The purpose of this review is to provide a latest summary of biomarkers associated with endothelial cell activation in COVID-19 and offer mechanistic insights into the molecular basis of endothelial activation/dysfunction in macro- and micro-vasculature of COVID-19 patients. & Weng, Jp. The thermoregulation system includes the hypothalamus in the brain, as well as the sweat. In COVID-19 patients, heart failure and myocardial injury are frequent complications, underscoring the clinical utility of SGLT2 inhibitors [128]. However, conclusions need to be analyzed with caution due to small sample size [165]. eCollection 2023 Apr. SARS-CoV-2 crosses the blood-brain barrier accompanied with basement membrane disruption without tight junctions alteration. Effectiveness of therapeutic heparin versus prophylactic heparin on death, mechanical ventilation, or intensive care unit admission in moderately ill patients with covid-19 admitted to hospital: RAPID randomised clinical trial. Efficacy and mechanisms of traditional Chinese medicine for COVID-19: a systematic review. Phytother Res. 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]. Li F, Li J, Wang PH, Yang N, Huang J, Ou J, et al. 2020;8:462. Cells. 2012;36:5715. 2022;96:3441. Article The polypharmacological profile of metformin makes it a promising candidate drug to be repurposed for controlling inflammation tsunami in diabetic COVID-19 patients [124]. 2022, https://doi.org/10.1002/ptr.7574. Vassiliou AG, Kotanidou A, Dimopoulou I, Orfanos SE. 2021;107:2323. 2. 2020;145:111694. Med Intensiv. The American-European Consensus Conference definition of the acute respiratory distress syndrome is dead, long live positive end-expiratory pressure! Falleni M, Tosi D, Savi F, Chiumello D, Bulfamante G. Endothelial-mesenchymal transition in COVID-19 lung lesions. 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]. It can be complicated by arrhythmias or thromboembolic episodes. Fardman A, Zahger D, Orvin K, Oren D, Kofman N, Mohsen J, et al. Theranostics. Many patients with severe COVID-19 present with coagulation abnormalities that mimic other systemic coagulopathies associated with severe infections, such as disseminated intravascular coagulation (DIC) or thrombotic microangiopathy, but COVID-19 has distinct features. However, after SARS-CoV-2 infection, ECs are detached more quickly without efficient regeneration [20]. Role of traditional chinese medicine in treating severe or critical covid-19: a systematic review of randomized controlled trials and observational studies. The IL-1, IL-6, and TNF cytokine triad is associated with post-acute sequelae of COVID-19. Coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 infection represents an ongoing public health burden leading to extensive morbidity and mortality worldwide [1]. Zha D, Fu M, Qian Y. Vascular endothelial glycocalyx damage and potential targeted therapy in COVID-19. Adv Exp Med Biol. 2020;32:17687. A vicious cycle: in severe and critically Ill COVID-19 patients. 2022;9:826218. Reis G, Dos Santos Moreira-Silva EA, Silva DCM, Thabane L, Milagres AC, Ferreira TS, et al. Complement activation induces excessive T cell cytotoxicity in severe COVID-19. 2021;6:402. 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. Shao Y, Saredy J, Xu K, Sun Y, Saaoud F, Drummer CT, et al. 2022;140:22235. Combinatorial treatment of human ECs with TNF- and IFN- increased the expression of ACE2, the receptor mediating viral entry via JAK/STAT1 pathway [13]. Hence, abnormalities of thyroid dysfunction are important to evaluate in COVID-19 [ 4 ]. Therefore, emerging therapies targeting endothelial dysfunction and endotheliopathy are hopeful to ameliorate COVID-19 associated lung injury [25]. Int J Obes (2005). Barbosa LC, Gonalves TL, de Araujo LP, Rosario LVO, Ferrer VP. 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]. Inflammatory cytokines, such as IL-6, promotes JAK and STATs phosphorylation [145]. Signal Transduct Target Ther. Tissue Barriers. Sulodexide significantly improves endothelial dysfunction and alleviates chest pain and palpitations in patients with long-COVID-19: Insights From TUN-EndCOV study. In addition, we need to screen for atherosclerotic plaque formation in COVID-19 survivors, as there are no actual clinical data providing the causal relationship between COVID-19 and atherosclerosis. Front Med. Mental status changes and core temperature distinguish potentially fatal heat stroke from heat exhaustion. IL-1 is an important cytokine released during cytokine storm in COVID-19 as well as its post-acute sequelae [91, 139]. The levels of senescent markers, such as PAI-1, p21 and sirtuin-1 in the plasma and lung ECs are elevated. Diabetes/hyperglycemia further exacerbate pre-existing endothelial dysfunction and hyperinflammation in COVID-19 patients. 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]. 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. 2) [2, 16]. Saviano A, Baumert TF. It represents a potential biomarker for monitoring disease progression in COVID-19 patients [112]. Like other types of organ injury, SARS-CoV-2 infection causes AKI by both direct and indirect mechanisms, including endotheliitis, thrombosis and glucolipid derangement. Thermoregulatory disorders and illness related to heat and - PubMed 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. According to the American-European Consensus Conference on acute respiratory distress syndrome (ARDS), the ARDS is the most severe form of the acute lung injury [17] as well as ongoing COVID-19 associated lethality [18]. Front Immunol. Qian Y, Lei T, Patel PS, Lee CH, Monaghan-Nichols P, Xin HB, et al. Front Environ Sci Eng. 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]. These include tachycardia, shortness of breath, fatigue and post-exercise exhaustion. 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]. 2022: 1-10. Cell Biosci. Excessive production of mtROS causes oxidative stress that perpetuates ECs inflammation, senescence and dysfunction. PubMedGoogle Scholar. Effect of anakinra on mortality in patients with COVID-19: a systematic review and patient-level meta-analysis. Gupta A, Madhavan MV, Sehgal K, Nair N, Mahajan S, Sehrawat TS, et al. 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]. 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]. Signal Transduct Target Ther. Redox imbalance links COVID-19 and myalgic encephalomyelitis - PNAS
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