thermoregulatory dysfunction in 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]. The protective role of ACE2 agonism in suppressing angiogenesis and maintaining endothelial integrity in COVID-19 warrant further investigation [19]. The polypharmacological profile of metformin makes it a promising candidate drug to be repurposed for controlling inflammation tsunami in diabetic COVID-19 patients [124]. Anakinra, by blocking interleukin 1 receptor, prevented VE-cadherin downregulation and lung vascular leakage. Cardiovasc Res. Han T, Ma S, Sun C, Zhang H, Qu G, Chen Y, et al. PubMed Central 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). 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]. 2021;12:653110. 2020;7:629413. Trends Microbiol. 2022;167:926. The post-COVID-19 cardiovascular autonomic dysfunction can affect global circulatory control, producing not only a POTS-like pattern but also tachycardia at rest, blood pressure instability with . Hu B, Huang S, Yin L. The cytokine storm and COVID-19. Front Cardiovasc Med. A significant proportion of people who test positive for COVID-19 have chemosensory deficits. 2012;36:5715. Mechanistically, fluvoxamine is a sigma-1 receptor (S1R) agonist which, on the one hand, reduces the expression of IL-6, while increasing that of eNOS. 2021;19:5. 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. To this end, lactate production from glycolysis pathway serves as a useful biomarker of EC barrier dysfunction [106]. Semin Thrombosis Hemost. Nogueira RC, Minnion M, Clark AD, Dyson A, Tanus-Santos JE, Feelisch M. On the origin of nitrosylated hemoglobin in COVID-19: Endothelial NO capture or redox conversion of nitrite? Effects of Shuanghuanglian oral liquids on patients with COVID-19: a randomized, open-label, parallel-controlled, multicenter clinical trial. Metformin in cardiovascular diabetology: a focused review of its impact on endothelial function. Slider with three articles shown per slide. 2021;95:e0139621. Metformin represents the first-line therapy for T2DM [123]. Vassiliou AG, Keskinidou C, Jahaj E, Gallos P, Dimopoulou I, Kotanidou A, et al. Kang X, Jin D, Jiang L, Zhang Y, Zhang Y, An X, et al. 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]. 2021;13:2209. Epub 2023 Jan 6. Bhowmik KK, Barek MA, Aziz MA, Islam MS. Impact of high-dose vitamin C on the mortality, severity, and duration of hospital stay in COVID-19 patients: a meta-analysis. Pang J, Xu F, Aondio G, Li Y, Fumagalli A, Lu M, et al. Copyright 2016 The Author. 2021;31:e12997. The SARS-CoV-2 main protease M(pro) causes microvascular brain pathology by cleaving NEMO in brain endothelial cells. The endothelium, the widely-distributed organ of the human body, is essential for maintaining tissue homeostasis by producing a variety of vasoactive molecules. Based on the evidence presented, there was heterogenous ACE2 expression in ECs from various vascular beds. FASEB J. 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. Satarker S, Tom AA, Shaji RA, Alosious A, Luvis M, Nampoothiri M. JAK-STAT pathway inhibition and their implications in COVID-19 therapy. Among these physiological functions, nitric oxide (NO) represents the key mechanism for maintaining endothelial homeostasis [2, 15]. 2022, https://doi.org/10.1002/ptr.7574. Kang S, Kishimoto T. Interplay between interleukin-6 signaling and the vascular endothelium in cytokine storms. However, several JAK/STAT inhibitors such as ruxolitinib, tofacitinib and baricitinib can suppress cytokine signaling cascade. 2021;163:15362. 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. Am J Respir Crit Care Med. & Weng, Jp. SARS-CoV-2 spike promotes inflammation and apoptosis through autophagy by ROS-suppressed PI3K/AKT/mTOR signaling. Blood. Henry BM, de Oliveira MHS, Cheruiyot I, Benoit JL, Cooper DS, Lippi G, et al. ACE2 angiotensin-converting enzyme-2, AXL AXL receptor tyrosine kinase, EndoMT endothelial-to-mesenchymal transition, NO nitric oxide, SASP senescence-associated secretory phenotype. 2021;34:812. Unexpectedly, propensity score-weighted analysis showed that treatment with ACEI/ARB was not significantly associated with the occurrence of defined end-points. 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]. April 27, 2023 - A new study shows that people with long COVID respond differently to COVID vaccines and that the condition may be caused by a dysfunction of the immune system -- possibly . Eur Respir J. 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. 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. Int J Infect Dis. 2021;58:457587. 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. Huang P, Zuo Q, Li Y, Oduro PK, Tan F, Wang Y, et al. sharing sensitive information, make sure youre on a federal 2020;10:2045894020966547. Glycocalyx protein component can be degraded by degrading enzyme such as heparinase. However, pre-treatment of ECs with losartan (belonging to ARB) and lisinopril (belonging to ACEI), fail to affect the susceptibility of hEC to SARS-CoV-2 infection [131]. Physiological functions of the vascular endothelium include: (1) maintenance of barrier integrity; (2) regulation of vascular tone; (3) regulation of hemostasis; (4) maintenance of an anti-inflammatory, anti-oxidant and anti-thrombotic interface; (5) regulation of anti-proliferative properties, and (6) regulation of cellular metabolism of ATP, glucose, amino acids, etc. Possible involvement of Syndecan-1 in the state of COVID-19 related to endothelial injury. Therefore, emerging therapies targeting endothelial dysfunction and endotheliopathy are hopeful to ameliorate COVID-19 associated lung injury [25]. Mortality of COVID-19 patients is increased by comorbidities of cardiovascular disease and hypertension in particular. Thermoregulation and afterdrop during hypothermia in patients with poikilothermia. 2022;3:100663. Villar J, Kacmarek RM. CAS Heat exhaustion; Heat stroke; Hypohidrosis; Hypothermia; Rewarming; Small fiber neuropathy; Thermoregulation. Fluvoxamine vs placebo and clinical deterioration in outpatients with symptomatic COVID-19: a randomized clinical trial. The net consequence is the extravasation of inflammatory and immune cell infiltrations [74]. Chem-Biol Interact. The elevated VEGF-A level further promotes endothelial leakage and inflammatory cell infiltration [19]. 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. Circulation. Introduction PubMed 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]. Tissue Barriers. CAS 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]. J Neuroinflammation. Cell Mol Life Sci. Consistent with this notion, elevated level of C3a in severe COVID-19 patients induced the activation of CD16+ cytotoxic T cells which promotes endothelial injury and the release of monocyte chemoattractant proteins as well as neutrophil activation [96]. Published evidence indicates that Severe Acute Respiratory Syndrome-Corona Virus (SARS-CoV-2) infection causes endothelial cell (EC) injury in the Coronavirus Disease 2019 (COVID-19). Pharmacological inhibition of senescence or SASP can reverse endothelial inflammation and leukocyte adhesion. ICU admission levels of endothelial biomarkers as predictors of mortality in critically Ill COVID-19 patients. Acta Pharmacol Sin. 2021;63:103182. 2020;222:178993. 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;321:L477l84. Pine AB, Meizlish ML, Goshua G, Chang CH, Zhang H, Bishai J, et al. ACE2 is a key regulator of RAAS by catalyzing the production of Ang-(17) from AngII, and the Ang-(17) can act on MAS receptor to combat the harmful effects caused by activation of RAAS[87, 130]. 2021;16:e0254167. SARS-CoV-2 infection relies on ACE2 expression in ECs [48]. Endothelial dysfunction, inflammation, and oxidative stress in COVID-19-mechanisms and therapeutic targets. 2021;107:2323. 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. 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]. Infection with various types of viruses, including SARS-CoV-2, can trigger endothelial senescence. Biomedicines. 82070464, 81941022, 81530025) and Strategic Priority Research Program of Chinese Academy of Sciences (Grant No. Sansone A, Jannini EA. Correspondence to Heparin prevents in vitro glycocalyx shedding induced by plasma from COVID-19 patients. ACE2 is an important component of the renin-angiotensin-aldosterone system (RAAS) by converting vasoactive AngII into Ang (17). However, compromised glycocalyx integrity promotes S protein/ACE2 interaction and facilitates viral entry [68]. Kondo Y, Larabee JL, Gao L, Shi H, Shao B, Hoover CM, et al. Acute brain dysfunction is highly prevalent in COVID-19 patients. 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. SARS-CoV-2 and COVID-19: The most important research questions. Direct or indirect mechanism after SARS-CoV-2 infection and the consequent endotheliitis/endotheliopathy incites multiple instances of endothelial dysfunction, including altered vascular tone, oxidative stress, inflammation/leukocyte adhesion, endothelial mesenchymal transition (EndoMT), mitochondria dysfunction, virus-induced senescence, cytokine storm, and coagulopathy [12, 13]. 2021;7:115665. 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. 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. Libby P, Lscher T. COVID-19 is, in the end, an endothelial disease. Qin H, Zhao A. Mesenchymal stem cell therapy for acute respiratory distress syndrome: from basic to clinics.

Melanie Lynskey Child, Quando Rondo Brother Name, Articles T

thermoregulatory dysfunction in covid 19

thermoregulatory dysfunction in covid 19