tetano
Editor, Senior Moderator
Life Sci
. 2022 Feb 8;294:120392.
doi: 10.1016/j.lfs.2022.120392. Online ahead of print.
The therapeutic potential of regulatory T cells in reducing cardiovascular complications in patients with severe COVID-19
Nafiseh Saghafi[SUP] 1 [/SUP], Seyed Abdolrahim Rezaee[SUP] 2 [/SUP], Amir Abbas Momtazi-Borojeni[SUP] 3 [/SUP], Fataneh Tavasolian[SUP] 4 [/SUP], Thozhukat Sathyapalan[SUP] 5 [/SUP], Elham Abdollahi[SUP] 6 [/SUP], Amirhossein Sahebkar[SUP] 7 [/SUP]
Affiliations
Abstract
The SARS coronavirus 2 (SARS CoV-2) causes Coronavirus Disease (COVID-19), is an emerging viral infection. SARS CoV-2 infects target cells by attaching to Angiotensin-Converting Enzyme (ACE2). SARS CoV-2 could cause cardiac damage in patients with severe COVID-19, as ACE2 is expressed in cardiac cells, including cardiomyocytes, pericytes, and fibroblasts, and coronavirus could directly infect these cells. Cardiovascular disorders are the most frequent comorbidity found in COVID-19 patients. Immune cells such as monocytes, macrophages, and T cells may produce inflammatory cytokines and chemokines that contribute to COVID-19 pathogenesis if their functions are uncontrolled. This causes a cytokine storm in COVID-19 patients, which has been associated with cardiac damage. Tregs are a subset of immune cells that regulate immune and inflammatory responses. Tregs suppress inflammation and improve cardiovascular function through a variety of mechanisms. This is an exciting research area to explore the cellular, molecular, and immunological mechanisms related to reducing risks of cardiovascular complications in severe COVID-19. This review evaluated whether Tregs can affect COVID-19-related cardiovascular complications, as well as the mechanisms through which Tregs act.
Keywords: COVID-19; Cardiovascular complications; SARS CoV-2; Treatment; Tregs.
. 2022 Feb 8;294:120392.
doi: 10.1016/j.lfs.2022.120392. Online ahead of print.
The therapeutic potential of regulatory T cells in reducing cardiovascular complications in patients with severe COVID-19
Nafiseh Saghafi[SUP] 1 [/SUP], Seyed Abdolrahim Rezaee[SUP] 2 [/SUP], Amir Abbas Momtazi-Borojeni[SUP] 3 [/SUP], Fataneh Tavasolian[SUP] 4 [/SUP], Thozhukat Sathyapalan[SUP] 5 [/SUP], Elham Abdollahi[SUP] 6 [/SUP], Amirhossein Sahebkar[SUP] 7 [/SUP]
Affiliations
- PMID: 35149115
- DOI: 10.1016/j.lfs.2022.120392
Abstract
The SARS coronavirus 2 (SARS CoV-2) causes Coronavirus Disease (COVID-19), is an emerging viral infection. SARS CoV-2 infects target cells by attaching to Angiotensin-Converting Enzyme (ACE2). SARS CoV-2 could cause cardiac damage in patients with severe COVID-19, as ACE2 is expressed in cardiac cells, including cardiomyocytes, pericytes, and fibroblasts, and coronavirus could directly infect these cells. Cardiovascular disorders are the most frequent comorbidity found in COVID-19 patients. Immune cells such as monocytes, macrophages, and T cells may produce inflammatory cytokines and chemokines that contribute to COVID-19 pathogenesis if their functions are uncontrolled. This causes a cytokine storm in COVID-19 patients, which has been associated with cardiac damage. Tregs are a subset of immune cells that regulate immune and inflammatory responses. Tregs suppress inflammation and improve cardiovascular function through a variety of mechanisms. This is an exciting research area to explore the cellular, molecular, and immunological mechanisms related to reducing risks of cardiovascular complications in severe COVID-19. This review evaluated whether Tregs can affect COVID-19-related cardiovascular complications, as well as the mechanisms through which Tregs act.
Keywords: COVID-19; Cardiovascular complications; SARS CoV-2; Treatment; Tregs.