4.1 Review

Telomerase, Autophagy and Acute Kidney Injury

期刊

NEPHRON
卷 134, 期 3, 页码 145-148

出版社

KARGER
DOI: 10.1159/000446665

关键词

Telomerase T; Telomerase C; Renal ischemia reperfusion; Autophagy; Proximal tubule; Mammalian target of rapamycin; Senescence; p16

资金

  1. VA [5I01BX000320-07] Funding Source: Federal RePORTER
  2. NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK051265, R01DK062794, P30DK079337, R01DK095785, R24DK103067] Funding Source: NIH RePORTER
  3. Veterans Affairs [I01BX000320] Funding Source: NIH RePORTER
  4. NIDDK NIH HHS [R01 DK095785, R24 DK103067, R01 DK051265, R01 DK062794, P30 DK079337] Funding Source: Medline
  5. BLRD VA [I01 BX000320] Funding Source: Medline

向作者/读者索取更多资源

In humans, aging is associated with telomere shortening and increased susceptibility to acute kidney injury. Telomerase is essential to maintain telomere length. The fourth generation mice with telomerase deletion have progressive shortening of telomeres. Those mice delayed recovery from ischemia-reperfusion injury, due to an increase in tubule cell senescence and impairment of autophagy, the latter of which may be mediated in part by increased mTOR signaling. (C) 2016 S. Karger AG, Basel

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