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Cell life versus cell longevity: The mysteries surrounding the NAD(+) precursor nicotinamide

期刊

CURRENT MEDICINAL CHEMISTRY
卷 13, 期 8, 页码 883-895

出版社

BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/092986706776361058

关键词

Akt; Alzheimer's disease; apoptosis; caspases; diabetes; erythropoietin; Huntington's disease; microglia; NAD(+); Parkinson's disease; stroke; vitamin B-3

资金

  1. NIEHS NIH HHS [P30 ES06639, P30 ES006639] Funding Source: Medline
  2. NINDS NIH HHS [R01 NS053946-01A2, R01 NS053946] Funding Source: Medline
  3. NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [P30ES006639] Funding Source: NIH RePORTER
  4. NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS053946] Funding Source: NIH RePORTER

向作者/读者索取更多资源

Nicotinamide, the amide form of niacin (vitamin B-3), is file precursor for the coenzyme beta-nicotinamide adenine dinucleotide (NAD(+)) and plays a significant role during the enhancement of cell survival as well as cell longevity. Yet. these abilities of nicotinamide appear to be diametrically opposed. Here we describe the development of nicotinamide as a novel agent that is critical for modulating Cellular metabolism, plasticity. longevity, and inflammatory microglial function as well as for influencing cellular life span. The capacity of nicotinamide to govern not only intrinsic cellular integrity, but also extrinsic cellular inflammation rests with the modulation of a host of cellular targets that involve mitochondrial membrane potential, poly(ADP-ribose) polymerase. protein kinase B (Akt), Forkhead transcription factors, Bad. caspases, and microglial activation. Further knowledge acquired in regards to the ability of nicotinamide to foster cellular survival and regulate cellular lifespan should significantly promote the development of therapies against a host of disorders, such as aging, Alzheimer's disease, diabetes, cerebral ischemia, Parkinson's disease, and cancer.

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