Mitochondria in Renal Ischemia-Reperfusion Injury: From Mechanisms to Therapeutics - PubMed
5 hours ago
- #acute kidney injury
- #ischemia-reperfusion
- #mitochondria
- Renal ischemia-reperfusion injury (IRI) is a major cause of acute kidney injury (AKI), which has high global incidence and mortality.
- The kidney is highly dependent on mitochondrial integrity due to its high energy demands and mitochondrial content.
- Mitochondrial dysfunction during IRI involves ATP depletion, Ca2+ overload, mtROS production, loss of membrane potential, mPTP opening, mtDNA damage, and mtDAMP release.
- These mitochondrial disruptions amplify inflammation and trigger regulated cell-death pathways.
- Recent research highlights the importance of mitochondrial bioenergetics, quality control, and immune signaling in IRI-AKI.
- Potential therapeutic strategies include enhancing antioxidant defenses, improving mitochondrial quality control (biogenesis, dynamics, mitophagy), and modulating mtDAMP sensing.