ArticleMechanisms of ageing and development2010
High-affinity Na(+)-dependent dicarboxylate cotransporter promotes cellular senescence by inhibiting SIRT1.
Article in Mechanisms of ageing and development, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Liver-specific SLC13A3 modulation alleviates MASLD by regulating NADMolecular and cellular biochemistry · 2026Article
- Anti-Aging Drugs and the Related Signal Pathways.Biomedicines · 2024Review
- Blockage of glutamine-dependent anaplerosis affects mTORC1/2 activity and ultimately leads to cellular senescence-like response.Biology open · 2019Article
- Transient postnatal overfeeding causes liver stress-induced premature senescence in adult mice.Scientific reports · 2017Article
- Sodium-coupled dicarboxylate and citrate transporters from the SLC13 family.Pflugers Archiv : European journal of physiology · 2014Review
- SIRT3 overexpression antagonizes high glucose accelerated cellular senescence in human diploid fibroblasts via the SIRT3-FOXO1 signaling pathway.Age (Dordrecht, Netherlands) · 2013Article
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11 authors at 1 institution in 1 country.
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Abstract
High-affinity Na(+)-dependent dicarboxylate cotransporter (NaDC3) can transport Krebs cycle intermediates into cells. Our previous study has shown that NaDC3 promotes cellular senescence, but its mechanism is not clear. It is known that when the concentration of intermediates in Krebs cycle is increased, NAD(+)/NADH ratio will be decreased. NAD(+)-dependent histone deacetylase sirtuin1 (SIRT1) prolongs mammalian cellular lifespan. Therefore, we propose that NaDC3 accelerates cellular aging by inhibiting SIRT1. After NaDC3 was overexpressed in two human embryo lung fibroblastic cell lines, WI38 and MRC-5, we found that the cells displayed aging-related phenotypes in advance. Meanwhile, the level of SIRT1 activity was down-regulated. In WI38/hNaDC3 cells treated with the activators of SIRT1, aging-related phenotypes induced by NaDC3 were obviously improved. The NAD(+)/NADH ratio in WI38/hNaDC3 cells was also decreased. Further study found that enhanced intracellular NAD(+) level could attenuate the aging phenotypes induced by NaDC3. Thus, NaDC3 promotes cellular senescence probably by inhibiting NAD(+)-dependent SIRT1.
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