ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2012
Calcium/calmodulin-dependent protein kinase IV limits organ damage in hepatic ischemia-reperfusion injury through induction of autophagy.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 54 citations in OpenAlex.
- Central role for MCP-1/CCL2 in injury-induced inflammation revealed by in vitro, in silico, and clinical studies.PloS one · 2013Trial
- Exploratory Gene Expression Profiling of Cisplatin-Induced Neurotoxicity in Rat Brain.International journal of molecular sciences · 2025Article
- Sepsis restructures the mitochondrial calcium uniporter complex in the lymphoid tissues of mice and humans.Communications biology · 2025Article
- Mechanistic Implications of GSK and CREB Crosstalk in Ischemia Injury.Neurotoxicity research · 2023Review
- Autophagy in liver diseases.World journal of hepatology · 2021Review
- CaMKIV regulates mitochondrial dynamics during sepsis.Cell calcium · 2020Article
- In vitro treatment of 3 T3-L1 adipocytes with recombinant Calcium/calmodulin-dependent Protein Kinase IV (CaMKIV) limits ER stress and improves insulin sensitivity through inhibition of autophagy via the mTOR/CREB signaling pathway.BMC endocrine disorders · 2020Article
- Calmodulin-mediated events during the life cycle of the amoebozoan Dictyostelium discoideum.Biological reviews of the Cambridge Philosophical Society · 2020Review
- Ischaemia reperfusion injury in liver transplantation: Cellular and molecular mechanisms.Liver international : official journal of the International Association for the Study of the Liver · 2019Review
- GSK-3β mediates ischemia-reperfusion injury by regulating autophagy in DCD liver allografts.International journal of clinical and experimental pathology · 2019Article
- Calcium/calmodulin-dependent protein kinase IV (CaMKIV) activation contributes to the pathogenesis of experimental colitis via inhibition of intestinal epithelial cell proliferation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- cGAS-mediated autophagy protects the liver from ischemia-reperfusion injury independently of STING.American journal of physiology. Gastrointestinal and liver physiology · 2018Article
- Calcium Signaling in Liver Injury and Regeneration.Frontiers in medicine · 2018Review
- Calcium/calmodulin-dependent protein kinase regulates the PINK1/Parkin and DJ-1 pathways of mitophagy during sepsis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Article
- Quercetin Pretreatment Attenuates Hepatic Ischemia Reperfusion-Induced Apoptosis and Autophagy by Inhibiting ERK/NF-Gastroenterology research and practice · 2017Article
- The Activation and Function of Autophagy in Alcoholic Liver Disease.Current molecular pharmacology · 2017Review
- Protective benefits of AMP-activated protein kinase in hepatic ischemia-reperfusion injury.American journal of translational research · 2017Review
- Blue light reduces organ injury from ischemia and reperfusion.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Autophagy and liver ischemia-reperfusion injury.BioMed research international · 2015Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Sterile inflammatory insults, such as ischemia-reperfusion (I/R) injury, result from pathogenic factors, including damage-associated molecular pattern signaling, activation of innate immunity, and upregulation of proinflammatory cytokines. At the same time, a number of protective, or prosurvival, pathways are also activated, and the extent of end-organ damage is ultimately determined by the balance between these two systems. In liver I/R, members of the calcium/calmodulin-dependent protein kinase (CaMK) family are known to be activated, but their individual roles are largely unknown. In this study, we show that one CaMK member, CaMKIV, is protective in hepatic I/R by activating the prosurvival pathway of autophagy in hepatocytes. CaMKIV knockout mice experience significantly worse organ damage after I/R and are deficient in hepatocyte autophagic signaling. Restoration of autophagic signaling with rapamycin reduces organ damage in CaMKIV knockout mice to wild-type levels. In vitro, we show that CaMKIV activation induces autophagy in mouse hepatocytes, and that CaMKIV activation protects hepatocytes from oxidative stress-induced cell death. In conclusion, the protective autophagic signaling pathway serves to reduce organ damage following I/R and is regulated by activation of CaMKIV signaling in hepatocytes.
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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.