TY - JOUR
T1 - IMPLICATIONS OF THE NADASE CD38 IN COVID PATHOPHYSIOLOGY
AU - Zeidler, Julianna D.
AU - Kashyap, Sonu
AU - Hogan, Kelly A.
AU - Chini, Eduardo Nunes
N1 - Publisher Copyright:
© 2022 the American Physiological Society.
PY - 2022/1
Y1 - 2022/1
N2 - During the COVID-19 pandemic, efforts have been made worldwide to develop effective therapies to address the devastating immune-mediated effects of SARS-CoV-2. With the exception of monoclonal antibody-mediated therapeutics and preventive approaches such as mass immunization, most experimental or repurposed drugs have failed in large randomized clinical trials (https://www.who.int/publications/i/item/therapeutics-and-covid-19-living-guideline). The worldwide spread of SARS-CoV-2 virus revealed specific susceptibilities to the virus among the elderly and individuals with age-related syndromes. These populations were more likely to experience a hyperimmune response characterized by a treatment-resistant acute lung pathology accompanied by multiple organ failure. These observations underscore the interplay between the virus, the biology of aging, and outcomes observed in the most severe cases of SARS-CoV-2 infection. The ectoenzyme CD38 has been implicated in the process of “inflammaging” in aged tissues. In a current publication, Horenstein et al. present evidence to support the hypothesis that CD38 plays a central role in altered immunometabolism resulting from COVID-19 infection. The authors discuss a critical but underappreciated trifecta of CD38-mediated NAD1 metabolism, aging, and COVID-19 immune response and speculate that the CD38/NAD1 axis is a promising therapeutic target for this disease.
AB - During the COVID-19 pandemic, efforts have been made worldwide to develop effective therapies to address the devastating immune-mediated effects of SARS-CoV-2. With the exception of monoclonal antibody-mediated therapeutics and preventive approaches such as mass immunization, most experimental or repurposed drugs have failed in large randomized clinical trials (https://www.who.int/publications/i/item/therapeutics-and-covid-19-living-guideline). The worldwide spread of SARS-CoV-2 virus revealed specific susceptibilities to the virus among the elderly and individuals with age-related syndromes. These populations were more likely to experience a hyperimmune response characterized by a treatment-resistant acute lung pathology accompanied by multiple organ failure. These observations underscore the interplay between the virus, the biology of aging, and outcomes observed in the most severe cases of SARS-CoV-2 infection. The ectoenzyme CD38 has been implicated in the process of “inflammaging” in aged tissues. In a current publication, Horenstein et al. present evidence to support the hypothesis that CD38 plays a central role in altered immunometabolism resulting from COVID-19 infection. The authors discuss a critical but underappreciated trifecta of CD38-mediated NAD1 metabolism, aging, and COVID-19 immune response and speculate that the CD38/NAD1 axis is a promising therapeutic target for this disease.
KW - CD38
KW - COVID-19
KW - Inflammation
KW - NAD
KW - Nicotinamide adenine dinucleotide
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U2 - 10.1152/physrev.00007.2021
DO - 10.1152/physrev.00007.2021
M3 - Review article
C2 - 34494892
AN - SCOPUS:85121906942
SN - 0031-9333
VL - 102
SP - 339
EP - 341
JO - Physiological Reviews
JF - Physiological Reviews
IS - 1
ER -