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The therapeutic potential of regulatory T cells in reducing cardiovascular complications in patients with severe COVID-19.
Saghafi, Nafiseh; Rezaee, Seyed Abdolrahim; Momtazi-Borojeni, Amir Abbas; Tavasolian, Fataneh; Sathyapalan, Thozhukat; Abdollahi, Elham; Sahebkar, Amirhossein.
  • Saghafi N; Department of Gynecology, Woman Health Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
  • Rezaee SA; Department of Immunology and Allergy, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran; Research Center for HIV/AIDS, HTLV and Viral Hepatitis, Iranian Academic Center for Education, Culture and Research (ACECR), Mashhad Branch, Mashhad, Iran; Inflammation and Inflammatory D
  • Momtazi-Borojeni AA; Department of Medical Biotechnology and Nanotechnology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
  • Tavasolian F; Toronto Western Hospital, Toronto, Canada.
  • Sathyapalan T; Academic Diabetes, Endocrinology and Metabolism, Hull York Medical School, University of Hull, UK.
  • Abdollahi E; Department of Gynecology, Woman Health Research Center, Mashhad University of Medical Sciences, Mashhad, Iran; Department of Immunology and Allergy, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Electronic address: Abdollahie@mums.ac.ir.
  • Sahebkar A; Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran; Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran; School of Medicine, The University of Western Australia, Perth, Australia; Department
Life Sci ; 294: 120392, 2022 Apr 01.
Article in English | MEDLINE | ID: covidwho-1670857
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.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Cardiovascular Diseases / T-Lymphocytes, Regulatory / SARS-CoV-2 / COVID-19 Type of study: Experimental Studies / Prognostic study Limits: Animals / Humans Language: English Journal: Life Sci Year: 2022 Document Type: Article Affiliation country: J.lfs.2022.120392

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Cardiovascular Diseases / T-Lymphocytes, Regulatory / SARS-CoV-2 / COVID-19 Type of study: Experimental Studies / Prognostic study Limits: Animals / Humans Language: English Journal: Life Sci Year: 2022 Document Type: Article Affiliation country: J.lfs.2022.120392