| First Author | Hine C | Year | 2015 |
| Journal | Cell | Volume | 160 |
| Issue | 1-2 | Pages | 132-44 |
| PubMed ID | 25542313 | Mgi Jnum | J:219291 |
| Mgi Id | MGI:5620063 | Doi | 10.1016/j.cell.2014.11.048 |
| Citation | Hine C, et al. (2015) Endogenous hydrogen sulfide production is essential for dietary restriction benefits. Cell 160(1-2):132-44 |
| abstractText | Dietary restriction (DR) without malnutrition encompasses numerous regimens with overlapping benefits including longevity and stress resistance, but unifying nutritional and molecular mechanisms remain elusive. In a mouse model of DR-mediated stress resistance, we found that sulfur amino acid (SAA) restriction increased expression of the transsulfuration pathway (TSP) enzyme cystathionine gamma-lyase (CGL), resulting in increased hydrogen sulfide (H2S) production and protection from hepatic ischemia reperfusion injury. SAA supplementation, mTORC1 activation, or chemical/genetic CGL inhibition reduced H2S production and blocked DR-mediated stress resistance. In vitro, the mitochondrial protein SQR was required for H2S-mediated protection during nutrient/oxygen deprivation. Finally, TSP-dependent H2S production was observed in yeast, worm, fruit fly, and rodent models of DR-mediated longevity. Together, these data are consistent with evolutionary conservation of TSP-mediated H2S as a mediator of DR benefits with broad implications for clinical translation. PAPERFLICK: |
