The NADase CD38 is induced by factors secreted from senescent cells providing a potential link between senescence and age-related cellular NAD + decline
Chini C., Hogan KA., Warner GM., Tarragó MG., Peclat TR., Tchkonia T.
Animal Study, published in Biochem Biophys Res Commun (2019) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Biochem Biophys Res Commun (2019)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 30975470
- PMCID
- PMC6486859
- DOI
- 10.1016/j.bbrc.2019.03.199
- Citations
- 109
Abstract (original English)
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.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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