ArticleNephron. Experimental nephrology2014
Beneficial Effects of AMP-Activated Protein Kinase Agonists in Kidney Ischemia-Reperfusion: Autophagy and Cellular Stress Markers.
Article in Nephron. Experimental nephrology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 52 citations in OpenAlex.
- AMP-dependent kinase stimulates the expression of αKlotho.FEBS open bio · 2024Article
- Mutation of regulatory phosphorylation sites in PFKFB2 does not affect the anti-fibrotic effect of metformin in the kidney.PloS one · 2023Article
- Polyethylene glycol capped gold nanoparticles ameliorate renal ischemia-reperfusion injury in diabetic mice through AMPK-Nrf2 signaling pathway.Environmental science and pollution research international · 2022Article
- Mitochondria as mediators of systemic inflammation and organ cross talk in acute kidney injury.American journal of physiology. Renal physiology · 2022Review
- Metformin protects against cardiac and renal damage in diabetic cardiac arrest patients.Resuscitation · 2022Article
- Sirtuin 5 depletion impairs mitochondrial function in human proximal tubular epithelial cells.Scientific reports · 2021Article
- Use of Anti-Diabetic Agents in Non-Diabetic Kidney Disease: From Bench to Bedside.Life (Basel, Switzerland) · 2021Review
- Immune Modulation as a Key Mechanism for the Protective Effects of Remote Ischemic Conditioning After Stroke.Frontiers in neurology · 2021Review
- Patulin suppresses αScientific reports · 2020Article
- Activation of the AMP-related kinase (AMPK) induces renal vasodilatation and downregulates Nox-derived reactive oxygen species (ROS) generation.Redox biology · 2020Article
- Review
- Molecular strategies used by hibernators: Potential therapeutic directions for ischemia reperfusion injury and preservation of human donor organs.Transplantation reviews (Orlando, Fla.) · 2020Review
- Metabolic Flexibility and Innate Immunity in Renal Ischemia Reperfusion Injury: The Fine Balance Between Adaptive Repair and Tissue Degeneration.Frontiers in immunology · 2020Review
- Amniotic fluid stem cells ameliorate cisplatin-induced acute renal failure through induction of autophagy and inhibition of apoptosis.Stem cell research & therapy · 2019Article
- Metformin: A Candidate Drug for Renal Diseases.International journal of molecular sciences · 2018Review
- A comparison of LKB1/AMPK/mTOR metabolic axis response to global ischaemia in brain, heart, liver and kidney in a rat model of cardiac arrest.BMC cell biology · 2018Article
- Aged kidney: can we protect it? Autophagy, mitochondria and mechanisms of ischemic preconditioning.Cell cycle (Georgetown, Tex.) · 2018Article
- Proteasome and Organs Ischemia-Reperfusion Injury.International journal of molecular sciences · 2017Review
- Suppressed autophagic response underlies augmentation of renal ischemia/reperfusion injury by type 2 diabetes.Scientific reports · 2017Article
- Drp1-dependent mitophagy protects against cisplatin-induced apoptosis of renal tubular epithelial cells by improving mitochondrial function.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 3 countries.
Funding
Abstract
Background: Kidney ischemia-reperfusion is a form of acute kidney injury resulting in a cascade of cellular events prompting rapid cellular damage and suppression of kidney function. A cellular response to ischemic stress is the activation of AMP-activated protein kinase (AMPK), where AMPK induces a number of homeostatic and renoprotective mechanisms, including autophagy. However, whether autophagy is beneficial or detrimental in ischemia-reperfusion remains controversial. We investigated the effects of agonist induction of AMPK activity on autophagy and cell stress proteins in the model of kidney ischemia-reperfusion. Methods: AMPK agonists, AICAR (0.1 g/kg) and metformin (0.3 g/kg), were administered 24 h prior to ischemia, with kidneys harvested at 24 h of reperfusion. Results: We observed a paradoxical decrease in AMPK activity accompanied by increases in mammalian target of rapamycin (mTOR) C1 activity and p62/SQSTM1 expression. These results led us to propose that AMPK and autophagy are insufficient to properly counter the cellular insults in ischemia-reperfusion. Agonist induction of AMPK activity with AICAR or metformin increased macroautophagy protein LC3 and normalized p62/SQSTM1 expression and mTOR activity. Ischemia-reperfusion increases in Beclin-1 and PINK1 expressions, consistent with increased mitophagy, were also mitigated with AMPK agonists. Stress-responsive and apoptotic marker expressions increase in ischemia-reperfusion and are significantly attenuated with agonist administration, as are early indicators of fibrosis. Conclusions: Our data suggest that levels of renoprotective AMPK activity and canonical autophagy are insufficient to maintain cellular homeostasis, contributing to the progression of ischemia-reperfusion injury. We further demonstrate that induction of AMPK activity can provide beneficial cellular effects in containing injury in ischemia-reperfusion. © 2014 S. Karger AG, Basel.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.