ArticleOncotarget2017
FAM3A mediates PPARγ's protection in liver ischemia-reperfusion injury by activating Akt survival pathway and repressing inflammation and oxidative stress.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- Hydrogen Regulates Ulcerative Colitis by Affecting the Intestinal Redox Environment.Journal of inflammation research · 2024Review
- Unveiling the Crucial Roles of OJournal of the American Chemical Society · 2023Article
- Effect of the Non-steroidal Anti-inflammatory Drug Diclofenac on Ischemia-Reperfusion Injury in Rat Liver: A Nitric Oxide-Dependent Mechanism.Inflammation · 2023Article
- FAM3A mediates the phenotypic switch of human aortic smooth muscle cells stimulated with oxidised low-density lipoprotein by influencing the PI3K-AKT pathway.In vitro cellular & developmental biology. Animal · 2023Article
- Resveratrol promotes liver cell survival in mice liver-induced ischemia-reperfusion through unfolded protein response: a possible approach in liver transplantation.BMC pharmacology & toxicology · 2022Article
- Intracellular ATP Signaling Contributes to FAM3A-Induced PDX1 Upregulation in Pancreatic Beta Cells.Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association · 2022Article
- ATP Secretion and Metabolism in Regulating Pancreatic Beta Cell Functions and Hepatic Glycolipid Metabolism.Frontiers in physiology · 2022Review
- Novel Targets and Therapeutic Strategies to Protect Against Hepatic Ischemia Reperfusion Injury.Frontiers in medicine · 2021Review
- PPARγ in Ischemia-Reperfusion Injury: Overview of the Biology and Therapy.Frontiers in pharmacology · 2021Review
- Repurposing Doxepin to Ameliorate Steatosis and Hyperglycemia by Activating FAM3A Signaling Pathway.Diabetes · 2020Article
- Analysis of miRNAs and their target genes associated with mucosal damage caused by transport stress in the mallard duck intestine.PloS one · 2020Article
- FOXO1 inhibition prevents renal ischemia-reperfusion injury via cAMP-response element binding protein/PPAR-γ coactivator-1α-mediated mitochondrial biogenesis.British journal of pharmacology · 2020Article
- FAM3A - A mitochondrial route to the stimulation of angiogenesis?EBioMedicine · 2019Article
- Endothelial microvesicles in hypoxic hypoxia diseases.Journal of cellular and molecular medicine · 2018Review
- Novel Targets for Treating Ischemia-Reperfusion Injury in the Liver.International journal of molecular sciences · 2018Review
- Protective role of puerarin on LPS/D-Gal induced acute liver injury via restoring autophagy.American journal of translational research · 2018Article
- Effects of initiating time and dosage ofWorld journal of gastroenterology · 2017Article
- FAM3C activates HSF1 to suppress hepatic gluconeogenesis and attenuate hyperglycemia of type 1 diabetic mice.Oncotarget · 2017Article
- FAM3A: a novel mitochondrial protein for the treatment of ischemic diseases.Cell cycle (Georgetown, Tex.)Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FAM3A is a novel mitochondrial protein, and its biological function remains largely unknown. This study determined the role and mechanism of FAM3A in liver ischemia-reperfusion injury (IRI). In mouse liver after IRI, FAM3A expression was increased. FAM3A-deficient mice exhibited exaggerated liver damage with increased serum levels of AST, ALT, MPO, MDA and oxidative stress when compared with WT mice after liver IRI. FAM3A-deficient mouse livers had a decrease in ATP content, Akt activity and anti-apoptotic protein expression with an increase in apoptotic protein expression, inflammation and oxidative stress when compared WT mouse livers after IRI. Rosiglitazone pretreatment protected against liver IRI in wild type mice but not in FAM3A-deficient mice. In cultured hepatocytes, FAM3A overexpression protected against, whereas FAM3A deficiency exaggerated oxidative stress-induced cell death. FAM3A upregulation or FAM3A overexpression inhibited hypoxia/reoxygenation-induced activation of apoptotic gene and hepatocyte death in P2 receptor-dependent manner. FAM3A deficiency blunted rosiglitazone's beneficial effects on Akt activation and cell survival in cultured hepatocytes. Collectively, FAM3A protects against liver IRI by activating Akt survival pathways, repressing inflammation and attenuating oxidative stress. Moreover, the protective effects of PPARγ agonist(s) on liver IRI are dependent on FAM3A-ATP-Akt pathway.
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