thermoregulatory dysfunction in covid 19

Biochimica et Biophysica Acta Mol Basis Dis. 2022. https://doi.org/10.1164/rccm.202207-1258ED. Direct or indirect mechanisms are operating to collectively indicate the alterations in vascular homeostasis in COVID-19 [54]. 2020;8:462. Mounting evidence suggests that SARS-CoV-2 infection leads to multiple instances of endothelial dysfunction, including reduced nitric oxide (NO) bioavailability, oxidative stress, endothelial injury, glycocalyx/barrier disruption, hyperpermeability, inflammation/leukocyte adhesion, senescence, endothelial-to-mesenchymal transition (EndoMT), hypercoagulability, thrombosis and many others. 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]. Cheng X, Liu YM, Li H, Zhang X, Lei F, Qin JJ, et al. Bauersachs J, de Boer RA, Lindenfeld J, Bozkurt B. Elevated expression of serum endothelial cell adhesion molecules in COVID-19 patients. (i) COVID-19 directly affects sustentacular (SUS) cells through interactions with the ACE2 receptor, thereby leading to abnormal transmission of odor molecules. 2) [2, 16]. However, the reported prevalence of these deficits in smell and taste varies widely, and the reason for the differences between studies is unclear. Correlation analysis indicates that the level of IL-6 positively correlated with the level of markers of endothelial activation (vWF, factor VIII, and D-dimer). Several clinical trials are ongoing to evaluate the safety and efficacy of JAK/STAT inhibitors [146]. 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]. Clipboard, Search History, and several other advanced features are temporarily unavailable. Thrombosis Res. When endothelial dysfunction/endotheliopathy/endotheliitis occurs in COVID-19, several markers of endothelial cell activation are used for assessing endothelial dysfunction in COVID-19 (Figs. For example, one study reported that primary human ECs express minimal level of ACE2 and the protease TMPRSS2, which limits their ability to generate highly infectious viral particles [50]. Oxid Med Cell Longev. Endothelial integrity is essential for maintaining the pulmonary capillary-alveolar barrier and lung homoeostasis. In addition, C-type lectin receptor L-SIGN, a receptor highly expressed on LSECs and lymphatic endothelial cells, was identified as the receptor for SARS-CoV-2 infection and may contribute to endotheliopathy in the liver [33]. 2021;6:266. Recent randomized clinical trials revealed that treatment with fluvoxamine (a selective serotonin reuptake inhibitors, SSRI) reduced the need for COVID-19 hospitalization, reduced mortality and improved outcome over 15 days [148,149,150]. 3). 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]. Anakinra, by blocking interleukin 1 receptor, prevented VE-cadherin downregulation and lung vascular leakage. Cells. Complement activation induces excessive T cell cytotoxicity in severe COVID-19. 2021;75:5035. Res Square. The infected cell releases danger signals leading to multiple aspects of endothelial dysfunction, which finally leads to impaired vascular activity and multi-organ injury. Fluvoxamine vs placebo and clinical deterioration in outpatients with symptomatic COVID-19: a randomized clinical trial. 2022;10:e42e51. Thus, metformin could be beneficial in reducing the mortality and composite outcomes in COVID-19 patients with T2DM [125]. 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]. A new study by investigators from the Smidt Heart Institute at Cedars-Sinai suggests long COVID-19 might be caused by a dysfunction of . The Erectile Dysfunction Drugs report tracks competitive progresses, strategies, mergers and acquisitions and new product development. 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]. FASEB J. Thermoregulation and afterdrop during hypothermia in patients with poikilothermia. 2021;41:176073. 2021;11:807691. It can be complicated by arrhythmias or thromboembolic episodes. Vasc Pharmacol. Vasculopathy in COVID-19. Thermoregulatory dysfunction is defined as significant loss of a person's capacity to control body temperature, and is associated with medical conditions that result in the person's health and bodily function being seriously affected when exposed to extremes of environmental temperatures. 2021;107:2323. Eligibility 2023 Mar 31;102(13):e33345. 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]. The primary pharmacological target of heparin could possibly be the endothelial glycocalyx, which is an important microstructure in endothelial cells, essential for maintaining vascular homeostasis by regulating vascular tone, barrier integrity, preventing leukocyte adhesion and thrombosis. Medications to protect and/or restore the endothelial glycocalyx integrity hold great therapeutic potential for COVID-19 associated glycocalyx disruption. Fiorentino G, Coppola A, Izzo R, Annunziata A, Bernardo M, Lombardi A, et al. COVID-19 and the cardiovascular system: implications for risk assessment, diagnosis, and treatment options. 2021;13:2209. Article 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]. Inhibition of heparanase by a non-anticoagulant heparin fragment prevented glycocalyx destruction in response to COVID-19 serum treatment [113]. PubMed Central Pulmonary capillary endothelium provides a fertile soil for viral entry, replication, thereby facilitating viral entry to the circulating blood [19, 20]. 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]. Eur J Clin Invest. The authors observed elevated levels of markers of coagulopathy/endotheliopathy and liver injury (ALT) in COVID-19 patients. Zhang L, Zhou L, Bao L, Liu J, Zhu H, Lv Q, et al. official website and that any information you provide is encrypted A review of acute limb ischemia in COVID-positive patients. Keywords: COVID-19; heat plan; heat stress; pandemic; personal protective equipment; sars-CoV-2; thermometry. 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. Pan R, Xie M, Chen M, Zhang Y, Ma J, Zhou J. MacKenzie MA, Hermus AR, Wollersheim HC, Binkhorst RA, Pieters GF. Thermoregulatory physiology sustains health by keeping body core temperature within a degree or two of 37C, which enables normal cellular function. A number of viral species, such as dengue, ebola and cytomegalovirus can infect endothelial cells (ECs) and cause endothelial dysfunction [5]. HIVC improves myocardial injury via decreasing biomarkers associated with inflammation in critically ill COVID-19 patients [155]. 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]. Amraei R, Rahimi N. COVID-19, Renin-Angiotensin system and endothelial dysfunction. 2021;164:6982. The elevated VEGF-A level further promotes endothelial leakage and inflammatory cell infiltration [19]. 2022;10:812. de Rooij L, Becker LM, Carmeliet P. A role for the vascular endothelium in post-acute COVID-19? Suzuki K, Okada H, Tomita H, Sumi K, Kakino Y, Yasuda R, et al. 2021;63:103182. Several large-scale clinical trials have suggested that glucocorticoid drug dexamethasone treatment is beneficial for COVID-19 patients [134]. Before Melatonin drugs inhibit SARS-CoV-2 entry into the brain and virus-induced damage of cerebral small vessels. These evidences signify their potential prognostic value to predict severity and mortality of COVID-19 [103, 107]. 2022;13:830061. 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. Ambrosino P, Calcaterra IL, Mosella M, Formisano R, DAnna SE, Bachetti T, et al. Papadopoulos KI, Sutheesophon W, Aw TC. 2021;47:3929. Theranostics. Qin H, Zhao A. Mesenchymal stem cell therapy for acute respiratory distress syndrome: from basic to clinics. J Hepatol. Circulation. Iwanski J, Kazmouz SG, Li S, Stansfield B, Salem TT, Perez-Miller S, et al. Acute kidney injury in severe COVID-19 has similarities to sepsis-associated kidney injury: a multi-omics study. 2021;64:103215. In addition to rehabilitation and exercise-based approaches [6], several categories of endothelium-targeted therapies have potential to ameliorate endothelial dysfunction in COVID-19 patients. Ngele MP, Haubner B, Tanner FC, Ruschitzka F, Flammer AJ. Endothelial dysfunction and thrombosis in patients with COVID-19-brief report. To obtain 2022 Dec 23;11(4):1728-1735. doi: 10.1002/fsn3.3202. Mitochondria is an important organelle that regulates antioxidant/redox signaling, by fine-tuning mitochondria-derived reactive oxygen species (mtROS) production. Kaundal RK, Kalvala AK, Kumar A. SARS-CoV-2 infection relies on ACE2 expression in ECs [48]. Data from randomized controlled clinical trials are scarce. The PAI-1 level in COVID-19 patients were as highly elevated compared with other cytokine release syndrome (sepsis or ARDS). Biomedicines. Kang X, Jin D, Jiang L, Zhang Y, Zhang Y, An X, et al. Ma Z, Yang KY, Huang Y, Lui KO. 2020;5:e138070. Markers of endothelial cell activation are associated with the severity of pulmonary disease in COVID-19. Forensic Sci Med Pathol. Front Med. Mansiroglu AK, Seymen H, Sincer I, Gunes Y. Endothelial to mesenchymal transition: a precursor to post-COVID-19 interstitial pulmonary fibrosis and vascular obliteration? Huet T, Beaussier H, Voisin O, Jouveshomme S, Dauriat G, Lazareth I, et al. Cardiovasc Res. 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. National Library of Medicine 2021;58:457587. Costa TJ, Potje SR, Fraga-Silva TFC, da Silva-Neto JA, Barros PR, Rodrigues D, et al. A vicious cycle: in severe and critically Ill COVID-19 patients. The pleiotropic effects of metformin help to control hyperglycemia, inhibit viral entry, and reduce inflammation following SARS-CoV-2 infection. Exp Mol Med. Internalization of SARS-CoV-2 also needs Neuropilin-1, a transmembrane protein with known angiogenic and immune-modulatory functions. Aging. Fodor A, Tiperciuc B, Login C, Orasan OH, Lazar AL, Buchman C, et al. doi: 10.1097/MD.0000000000033345. More recently, it is reported that thrombomodulin level was associated with augmented infiltration of immune cells in autopsy lung tissues [79], explaining the existence of thromboembolism in COVID-19 patients. 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]. EBioMedicine. 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. Targeting inflammation and cytokine storm in COVID-19. 2021;19:5. Charfeddine S, Ibnhadjamor H, Jdidi J, Torjmen S, Kraiem S, Bahloul A, et al. When endothelial dysfunction occurs, listed markers of endothelial dysfunction related to endothelial inflammation, thrombosis, glycocalyx damage, vascular tone are widely used. PLoS One. Onorato D, Pucci M, Carpene G, Henry BM, Sanchis-Gomar F, Lippi G. Protective effects of statins administration in European and North American patients infected with COVID-19: a meta-analysis. Matarese A, Gambardella J, Sardu C, Santulli G. miR-98 regulates TMPRSS2 expression in human endothelial cells: key implications for COVID-19. Taken together, the concerted actions of above factors lead to dysfunctional status of the vascular endothelium (endothelial dysfunction) (Fig. 2021;53:18695. Injury to the endothelial glycocalyx in critically Ill patients with COVID-19. Sci Immunol. Collectively, based on the multifaceted nature of endothelial dysfunction and complex patho-mechanisms of COVID-19, it warrants to be evaluated whether directly targeting endothelial dysfunction could result in a clinically significant improvement in outcome of COVID-19 patients. 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;16:e0253524. All the above evidence pinpoints the protective effect of heparin in COVID-19 could largely be attributable to glycocalyx-stabilizing effect. COVID-19 is also associated with liver injury. Vollenberg R, Tepasse PR, Ochs K, Floer M, Strauss M, Rennebaum F, et al. In the meantime, to ensure continued support, we are displaying the site without styles Front Med. Signal Transduct Target Ther. 2022;13:926189. world J mens health. J Virol. Georg P, Astaburuaga-Garca R, Bonaguro L, Brumhard S, Michalick L, Lippert LJ, et al. JAMA. The year in cardiovascular medicine 2021: heart failure and cardiomyopathies. COVID-19 is associated with pervasive ECs injury, increased capillary permeability, infiltration of inflammatory cells into perivascular tissues, interstitial edema and fluid retention in alveolar spaces [19]. Am J Physiol Lung Cell Mol Physiol. 2020;75:e1980. RNA-sequencing data further revealed the increased expression of markers of endothelial activation such as RELB (p50 subunit) and TNF- [65]. PubMed Int J Mol Sci. 2021;13:23424. Glycocalyx degradation and shedding disrupts endothelial junctional stability and plays a pivotal role in various forms of cardiovascular diseases [111]. Okada H, Yoshida S, Hara A, Ogura S, Tomita H. Vascular endothelial injury exacerbates coronavirus disease 2019: The role of endothelial glycocalyx protection. PLoS One. 2020;9:1652. Int J Mol Sci. Fang W, Jiang J, Su L, Shu T, Liu H, Lai S, et al. 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]. The fight against coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 infection is still raging. Thermoregulation is a vital function of the autonomic nervous system in response to cold and heat stress. 2020;202:117881. Cell Metab. 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]. 2021;276:119376. du Preez HN, Aldous C, Hayden MR, Kruger HG, Lin J. Pathogenesis of COVID-19 described through the lens of an undersulfated and degraded epithelial and endothelial glycocalyx. Severe COVID-19 patients had significantly higher levels of glycocalyx disruption (endocan and syndecan-1), endothelial damage (angiopoietin-2 and vWF), and inflammation (upregulation of soluble receptor for advanced glycation end-products, IL-6, ICAM-1 and VCAM-1). 5. Tomasa-Irriguible TM, Bielsa-Berrocal L. COVID-19: Up to 82% critically ill patients had low vitamin C values. 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]. CAS 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. There are multiple lines of evidences suggesting the involvement of endothelial dysfunction in COVID-19 [45]. 2020;2:e393e400. A recent study [35] has reported that IL-6 trans-signaling in LSECs leads to endotheliopathy and liver injury in COVID-19 patients. 2208085J08) and Local Innovative and Research Teams Project of Guangdong Pearl River Talents Program (Grant No. Direct activation of endothelial cells by SARS-CoV-2 nucleocapsid protein is blocked by simvastatin. SASP senescence-associated secretory phenotype. Cardiovasc Res. 2021;31:41532. Mechanistically, L-SIGN interacted with high-mannose-type N-glycans on the receptor-binding domain of SARS-CoV-2 spike protein in a Ca2+-dependent manner [33]. Six I, Guillaume N, Jacob V, Mentaverri R, Kamel S, Boullier A, et al. 2022;25:22540. Free Radic Biol Med. Ma L, Sahu SK, Cano M, Kuppuswamy V, Bajwa J, McPhatter J, et al. Zha D, Fu M, Qian Y. Vascular endothelial glycocalyx damage and potential targeted therapy in COVID-19. Eur Respir J. 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]. In the . Suo-wen Xu or Jian-ping Weng. 2020;56:2003167. 2012;36:5715. PubMed Int J Infect Dis. Frisoni P, Neri M, DErrico S, Alfieri L, Bonuccelli D, Cingolani M, et al. Heterogeneous ACE2 expression and endothelial damage was observed in COVID-19 autopsy tissues. Endothelial dysfunction as a primary consequence of SARS-CoV-2 Infection. Lopes-Paciencia S, Saint-Germain E, Rowell MC, Ruiz AF, Kalegari P, Ferbeyre G. The senescence-associated secretory phenotype and its regulation. ACE2 angiotensin-converting enzyme-2, TMPRSS2 transmembrane protease serine 2, ICAM-1 intercellular adhesion molecule 1, VCAM-1 vascular cell adhesion molecule 1, MCP1 monocyte chemoattractant protein-1, TGF- transforming growth factor , VEGF vascular endothelial growth factor, NO nitric oxide, IL-1 interleukin-1, IL-6 interleukin 6, TNF- tumor necrosis factor. 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]. 2020;7:629413. The role of NO in COVID-19 and potential therapeutic strategies. 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. Biering SB, de Sousa FTG, Tjang LV, Pahmeier F, Ruan R, Blanc SF, et al. Kang S, Kishimoto T. Interplay between interleukin-6 signaling and the vascular endothelium in cytokine storms. Jothimani D, Venugopal R, Abedin MF, Kaliamoorthy I, Rela M. COVID-19 and the liver. Role of angiotensin-converting enzyme 2 (ACE2) in COVID-19. Virus-induced senescence is a pathogenic trigger of endothelial dysfunction. Mechanistically, patients with heart failure demonstrate increased ACE2 gene and protein expression, suggesting that if patients with heart failure were infected by the virus, they are more susceptible to severe COVID-19 and develop into a critically-ill conditions [28]. Heat production and dissipation are dependent on a coordinated set of autonomic responses. The Sexual Long COVID (SLC): Erectile Dysfunction as a Biomarker of Systemic Complications for COVID-19 Long Haulers - PubMed. 2022;115:7783. Cytokine storm and histopathological findings in 60 cases of COVID-19-related death: from viral load research to immunohistochemical quantification of major players IL-1, IL-6, IL-15 and TNF-. 2022;23:6196. Anti-coagulatory or anti-hypertensive drugs treatment before admission leads to reduced number of CECs, indicating that COVID-19-associated coagulopathy and endotheliopathy could be ameliorated by anti-coagulatory or anti-hypertensive therapy [115]. Cardiovasc Res. While COVID-19 primarily affects the lungs, it also affects other organs, the heart in particular. In another study, nucleocapsid protein (NP) of SARS-CoV-2 promotes endothelial cell activation via the pro-inflammatory TLR2/NF-B and MAPK signaling pathways, which can be attenuated by simvastatin treatment. 2021;133:489507. Therapeutic potential of megadose vitamin C to reverse organ dysfunction in sepsis and COVID-19. Kumar N, Zuo Y, Yalavarthi S, Hunker KL, Knight JS, Kanthi Y, et al. The combination of multiple markers could afford better discriminative ability for diagnosis of coagulopathy and thromboembolism and are predictive of ICU admission in COVID-19 patients. Milani GP, Macchi M, Guz-Mark A. Vitamin C in the treatment of COVID-19. ACE2 angiotensin-converting enzyme-2, ACEI angiotensin converting enzyme inhibitors, ARB angiotensin receptor blockers, BRD4i bromodomain-containing protein 4 inhibitors, JAK janus kinase, SGLT2i sodium-glucose cotransporter-2 inhibitors. It is reported that COVID-19-patients had higher number of CECs than COVID-19-free subjects. Mol Med (Camb, Mass). Vigilance on new-onset atherosclerosis following SARS-CoV-2 infection. 2021;96:256175. The authors declare no competing interests. CAS Acta Pharmacol Sin. 2020;24:422. 2021;178:38648. 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. Google Scholar. It has been reported that the secretion of multiple markers of endothelial activation/dysfunction is elevated in COVID-19 patients, such as D-dimer (marker of coagulopathy and systemic thrombosis), vWF (a primary component of coagulation pathway and mediator of vascular inflammation and thrombo-inflammation released from Weibel-Palade bodies), factor VIII (marker of coagulation), PAI-1 (a marker of endothelial damage and senescence), soluble thrombomodulin (sTM), soluble P-selectin (marker of platelet and endothelial activation), soluble ICAM1 (sICAM1, marker of endothelial inflammation), soluble VCAM1 (sVCAM1, marker of endothelial inflammation), angiopoietin-2 (Ang-2, marker of angiogenesis and thrombosis), soluble E-selectin (sE-selectin, marker of endothelial inflammation), ET1 (a potent vasoconstrictor), VEGF-A (marker of angiogenesis and endothelial hyperpermeability), IL-6 and IL-8 (markers of endothelial inflammation), MCP-1 (marker of endothelial inflammation), resistin (an adipokine associated with endothelial damage and vasoconstriction), nitrosylhemoglobin (HbNO), lactate, and syndecan-1 (marker of endothelial glycocalyx damage) [19, 23, 80, 102,103,104,105,106]. In these cardiovascular complications, endothelial dysfunction plays a fundamental role [27]. Blood. Google Scholar. 2020;116:1097100. 2022;9:866113. These findings agree with a recent retrospective analysis by Zhang et al. 2021;15:70417. The pathophysiology, impact, and outcomes of hyperpyrexia in patients with COVID-19 have not yet been studied. The clinical detection of thermoregulatory impairment provides important diagnostic and localizing information in the evaluation of disorders that impair thermoregulatory pathways, including autonomic neuropathies and ganglionopathies. 2021;93:2506. This article reviews what is known about the effects of severe acute respiratory syndrome . Combinatorial treatment of human ECs with TNF- and IFN- increased the expression of ACE2, the receptor mediating viral entry via JAK/STAT1 pathway [13]. Int J Infect Dis. Endothelial senescence is an important aspect of endothelial dysfunction. Front Med. Chang R, Mamun A, Dominic A, Le NT. eCollection 2023 Apr. The PubMed wordmark and PubMed logo are registered trademarks of the U.S. Department of Health and Human Services (HHS). MeSH QJM. 2022;54:102362. ACE2 angiotensin-converting enzyme-2, AXL AXL receptor tyrosine kinase, EndoMT endothelial-to-mesenchymal transition, NO nitric oxide, SASP senescence-associated secretory phenotype. 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. https://doi.org/10.1038/s41401-022-00998-0, DOI: https://doi.org/10.1038/s41401-022-00998-0. Vasc Pharmacol. TCM has a well-documented safety profile in protecting against COVID-19 on the basis of standard care. However, the pathophysiology of acute and post-acute manifestations of COVID-19 (long COVID-19) is understudied. 2022;9:844228. 7). It remains to be investigated further whether TCM ameliorates COVID-19 partially by improving endothelial function. Evaluating the short-term effect of ambient temperature on non-fatal outdoor falls and road traffic injuries among children and adolescents in China: a time-stratified case-crossover study.

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