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10.1007/s00011-020-01372-8

http://scihub22266oqcxt.onion/10.1007/s00011-020-01372-8
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32529477!7289226!32529477
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suck abstract from ncbi


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pmid32529477      Inflamm+Res 2020 ; 69 (9): 825-839
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  • The possible pathophysiology mechanism of cytokine storm in elderly adults with COVID-19 infection: the contribution of "inflame-aging" #MMPMID32529477
  • Meftahi GH; Jangravi Z; Sahraei H; Bahari Z
  • Inflamm Res 2020[Sep]; 69 (9): 825-839 PMID32529477show ga
  • PURPOSE: Novel Coronavirus disease 2019 (COVID-19), is an acute respiratory distress syndrome (ARDS), which is emerged in Wuhan, and recently become worldwide pandemic. Strangely, ample evidences have been shown that the severity of COVID-19 infections varies widely from children (asymptomatic), adults (mild infection), as well as elderly adults (deadly critical). It has proven that COVID-19 infection in some elderly critical adults leads to a cytokine storm, which is characterized by severe systemic elevation of several pro-inflammatory cytokines. Then, a cytokine storm can induce edematous, ARDS, pneumonia, as well as multiple organ failure in aged patients. It is far from clear till now why cytokine storm induces in only COVID-19 elderly patients, and not in young patients. However, it seems that aging is associated with mild elevated levels of local and systemic pro-inflammatory cytokines, which is characterized by "inflamm-aging". It is highly likely that "inflamm-aging" is correlated to increased risk of a cytokine storm in some critical elderly patients with COVID-19 infection. METHODS: A systematic search in the literature was performed in PubMed, Scopus, Embase, Cochrane Library, Web of Science, as well as Google Scholar pre-print database using all available MeSH terms for COVID-19, Coronavirus, SARS-CoV-2, senescent cell, cytokine storm, inflame-aging, ACE2 receptor, autophagy, and Vitamin D. Electronic database searches combined and duplicates were removed. RESULTS: The aim of the present review was to summarize experimental data and clinical observations that linked the pathophysiology mechanisms of "inflamm-aging", mild-grade inflammation, and cytokine storm in some elderly adults with severe COVID-19 infection.
  • |*Aging[MESH]
  • |Adipocytes/cytology[MESH]
  • |Age Factors[MESH]
  • |Aged[MESH]
  • |Angiotensin II Type 2 Receptor Blockers/pharmacology[MESH]
  • |Autophagy[MESH]
  • |Betacoronavirus[MESH]
  • |COVID-19[MESH]
  • |Cellular Senescence[MESH]
  • |Coronavirus Infections/*immunology/*physiopathology[MESH]
  • |Cytokine Release Syndrome/*virology[MESH]
  • |Cytokines/immunology[MESH]
  • |Humans[MESH]
  • |Immune System[MESH]
  • |Inflammation/*immunology/physiopathology[MESH]
  • |Pandemics[MESH]
  • |Pneumonia, Viral/*immunology/*physiopathology[MESH]
  • |Reactive Oxygen Species/metabolism[MESH]
  • |Receptor, Angiotensin, Type 2/metabolism[MESH]
  • |SARS-CoV-2[MESH]
  • |Vitamin D Deficiency[MESH]


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