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The NADase CD38 is induced by factors secreted from senescent cells providing a potential link between senescence and age-related cellular NAD+ decline.


Maximus Peto’s Commentary

Ever since I learned that CD38 expression seems upregulated with aging, and its activity seems to be an important cause of the age-related decline in NAD+ with age, I have wondered: why does CD38 get upregulated? This study may have an answer to this question. This group reports that SASP factors secreted by senescent cells can upregulate CD38 in non-senescent cells. So one might suspect that serum NAD+ would increase after a round of senolytic treatment. I wonder whether anyone has assessed for that potential outcome after senolytics.


The NADase CD38 is induced by factors secreted from senescent cells providing a potential link between senescence and age-related cellular NAD+ decline.
Biochem Biophys Res Commun. 2019 May 28;513(2):486-493.
Chini C, Hogan KA, Warner GM, Tarragó MG, Peclat TR, Tchkonia T, Kirkland JL, Chini E
DOI: 10.1016/j.bbrc.2019.03.199
PubMed publication date (edat): 4/13/2019

Abstract

Tissue nicotinamide adenine dinucleotide (NAD+) decline has been implicated in aging. We have recently identified CD38 as a central regulator involved in tissue NAD+ decline during the aging process. CD38 is an ecto-enzyme highly expressed in endothelial and inflammatory cells. To date, the mechanisms that regulate CD38 expression in aging tissues characterized by the presence of senescent cells is not completely understood. Cellular senescence has been described as a hallmark of the aging process and these cells are known to secrete several factors including cytokines and chemokines through their senescent associated secretory phenotype (SASP). Here we investigated if the cellular senescence phenotype is involved in the regulation of CD38 expression and its NADase activity. We observed that senescent cells do not have high expression of CD38. However, the SASP factors secreted by senescent cells induced CD38 mRNA and protein expression and increased CD38-NADase activity in non-senescent cells such as endothelial cells or bone marrow derived macrophages. Our data suggest a link between cellular senescence and NAD+ decline in which SASP-mediated upregulation of CD38 can disrupt cellular NAD+ homeostasis.

PMID: 30975470
Free Full-Text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6486859/

Maximus Peto

Max Peto is a longevity researcher and founder of Long Life Labs. A biochemist by training, he studies the biochemistry of aging and longevity and has worked with research organizations such as SENS Research Foundation, Methuselah Foundation, BioAge Labs, Life Extension Foundation, and Ichor Therapeutics. His work at Long Life Labs is focused on empowering people to understand and manage the most critical factors for better health and longer life.

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