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Abstract
A steady increase in life expectancy has resulted in an equivalent increase in elderly patients who are more susceptible to diseases than young patients. In a recent study, we found that in both in vitro and in vivo models of ischemia/reperfusion (I/R), a loss of ATG4B is causatively associated with the increased sensitivity of the liver to I/R injury with age. Our work suggests that a restoration or enhancement of autophagy is a novel therapeutic modality to ameliorate liver function after I/R to aged livers.
Acknowledgments
This work was supported in part by the National Institutes of Health National Institute of Diabetes and Digestive and Kidney Diseases grant DK079879 (J.-S. K.) and National Institute on Aging AG 17994 (C.L.), AG 21042 (C.L.) and the University of Florida Institute on Aging, Claude D. Pepper Older Americans Independence Center (1 P30 AG028740).
Figures and Tables
Figure 1 Scheme of hepatocyte death after I/R in aged livers. Young livers have a robust autophagic responsiveness to mild stress, such as normoxia and starvation, as well as moderate ischemia/reperfusion (I/R). As a consequence of increased mitophagy that can eliminate abnormal or dysfunctional mitochondria in a timely manner, MPT onset and hepatocyte death do not occur in young livers. Despite a strong tolerance against mild stress, aged livers poorly tolerate I/R injury due to impaired autophagy, which in turn promotes the onset of the MPT and cell death.
Punctum to: Wang JH, Ahn IS, Fischer TD, Byeon JI, Dunn WA Jr, Behrns KE, et al. Autophagy suppresses age-dependent ischemia and reperfusion injury in livers of mice. Gastroenterology 2011; 141:2188 - 2199; e6 PMID: 21854730; http://dx.doi.org/10.1053/j.gastro.2011.08.005
