The DOI matches its Crossref record; 55 of the 55 references it cites were found in a registry or an index.
Nicotinamide-induced Mitophagy
Open accessAbstract
Active autophagy coupled with rapid mitochondrial fusion and fission constitutes an important mitochondrial quality control mechanism and is critical to cellular health. In our previous studies, we found that exposure of cells to nicotinamide causes a decrease in mitochondrial content and an increase in mitochondrial membrane potential (MMP) by activating autophagy and inducing mitochondrial fragmentation. Here, we present evidence to show that the effect of nicotinamide is mediated through an increase of the [NAD(+)]/[NADH] ratio and the activation of SIRT1, an NAD(+)-dependent deacetylase that plays a role in autophagy flux. The [NAD(+)]/[NADH] ratio was inversely correlated with the mitochondrial content, and an increase in the ratio by the mobilization of the malate-aspartate shuttle resulted in autophagy activation and mitochondrial transformation from lengthy filaments to short dots. Furthermore, treatment of cells with SIRT1 activators, fisetin or SRT1720, induced similar changes in the mitochondrial content. Importantly, the activators induced mitochondrial fragmentation only when SIRT1 expression was intact. Meanwhile, MMP did not increase when the cells were treated with the activators, suggesting that the change in MMP is not induced by the mitochondrial turnover per se and that elevation of the [NAD(+)]/[NADH] ratio may activate additional mechanisms that cause MMP augmentation. Together, our results indicate that a metabolic state resulting in an elevated [NAD(+)]/[NADH] ratio can modulate mitochondrial quantity and quality via pathways that may include SIRT1-mediated mitochondrial autophagy.
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“Autophagy is the major cellular mechanism removing organelles, including mitochondria, and along with coordinated mitochondrial fission and fusion is believed to selectively remove damaged (depolarized) mitochondria (7).”
BackgroundInfluentialhSIR2SIRT1 Functions as an NAD-Dependent p53 Deacetylase
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Small molecule activators of SIRT1 as therapeutics for the treatment of type 2 diabetes
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“lows: fisetin (3,7,3 ,4 -tetrahydroxyflavone), which is structurally and functionally similar to resveratrol and therefore suffers from the problem of off-target effects (38, 39), and SRT1720, which is known to be highly specific to SIRT1 (40).”
Background
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Cheng, S.-C., Quintin, J., Cramer, R. A., Shepardson, K. M., Saeed, S., Kumar, V., Giamarellos-Bourboulis, E. J., Martens, J. H. A., Rao, N. A., Aghajanirefah, A., et al. (2014) · Science · doi:10.1126/science.1250684 · Cited by 2,224
NAD+ metabolism and its roles in cellular processes during ageing
Covarrubias, A. J., Perrone, R., Grozio, A., & Verdin, E. (2021) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-020-00313-x · Cited by 1,617
Succinate: a metabolic signal in inflammation
Mills, E., & O’Neill, L. A. J. (2014) · Trends in Cell Biology · doi:10.1016/j.tcb.2013.11.008 · Cited by 741
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Jones, D. P., & Sies, H. (2015) · Antioxidants & Redox Signaling · doi:10.1089/ars.2015.6247 · Cited by 647
Metadata
- Authors
- Jang, S.-Y., Kang, H. T., & Hwang, E. S.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2012-06
- Volume
- 287
- Issue
- 23
- Pages
- 19304-19314
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2065991187
- Cited by
- 262
- References
- 55
- FWCI
- 9.69
- Type
- journal article
- Language
- en
- Open access
- hybrid
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