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Mitochondrial Telomerase Reverse Transcriptase Protects From Myocardial Ischemia/Reperfusion Injury by Improving Complex I Composition and Function.

Niloofar Ale-AghaPhilipp JakobsChristine GoyMark ZurekJulia RosenNadine Dyballa-RukesSabine MetzgerJan GreulichFlorian von AmelnOlaf EckermannKlaus UnfriedFedor BrackMaria GrandochMatthias ThielmannMarkus KamlerNilgün GedikPetra KleinbongardAndre HeinenGerd HeuschAxel GödeckeJoachim AltschmiedJudith Haendeler
Published in: Circulation (2021)
Mitochondrial, but not nuclear TERT, is critical for mitochondrial respiration and during ischemia/reperfusion injury. Mitochondrial TERT improves complex I subunit composition. TERT is present in human heart mitochondria, and remote ischemic preconditioning increases its level in those organelles. TA-65 has comparable effects ex vivo and improves the migratory capacity of endothelial cells and myofibroblast differentiation. We conclude that mitochondrial TERT is responsible for cardioprotection, and its increase could serve as a therapeutic strategy.
Keyphrases
  • oxidative stress
  • ischemia reperfusion injury
  • endothelial cells
  • heart failure
  • left ventricular
  • brain injury
  • transforming growth factor
  • subarachnoid hemorrhage
  • induced pluripotent stem cells
  • pulmonary fibrosis