ArticleHepatology (Baltimore, Md.)2022
Mitochondrial bioenergetics boost macrophage activation, promoting liver regeneration in metabolically compromised animals.
Article in Hepatology (Baltimore, Md.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
38 citing papers in PubMed, 58 citations in OpenAlex.
- Chlorogenic acid promotes liver regeneration after partial hepatectomy through activating Nrf2 via directly targeting Keap1.Acta pharmacologica Sinica · 2026Article
- Glutathione peroxidase 3 preserves hepatocyte mitochondrial quality control to enhance macrophage pro-regenerative phenotype during liver regeneration.Clinical and translational medicine · 2026Article
- Sensory Nerve-Derived CGRP Controls Osteoclastogenesis by Limiting Macrophage Bioenergetics in Bone Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Liver regeneration: cytokine regulation targeting hepatocytes and beyond.Life medicine · 2026Review
- Multidimensional regulation of hepatic macrophages in chronic liver disease: from metabolic reprogramming to intercellular and interorgan crosstalk.Frontiers in immunology · 2026Review
- Neutrophil-Mimicking Prussian blue nanozymes for synergistic targeted immuno-metabolic therapy of hepatic ischemia-reperfusion injury.Journal of nanobiotechnology · 2025Article
- Hypoxia-preconditioning human bone marrow-derived mesenchymal stem cells induce high-quality mitochondrial transfer through gap junctions to alleviate ischemia-reperfusion injury in liver graft.Cell communication and signaling : CCS · 2025Article
- Lipid metabolism orchestrates liver regeneration: an integrated metabolic network.Journal of translational medicine · 2025Review
- KYNA Ameliorates Hepatic Ischemia-Reperfusion Injury by Activating the Hippo Signalling Pathway via FTO-Dependent m6A Demethylation of LATS1.Cell proliferation · 2025Article
- Nanotechnology-driven advancements in organ transplantation: Multifaceted strategies for organ preservation, ischemia reperfusion injury, immunomodulation and post-transplant monitoring.Materials today. Bio · 2025Review
- TJ0113-induced mitophagy in acute liver failure detected by Raman microspectroscopy.Redox biology · 2025Article
- N6-Methyladenosine Modification in the Metabolic Dysfunction-Associated Steatotic Liver Disease.Nutrients · 2025Review
- Molecular mechanisms in liver repair and regeneration: from physiology to therapeutics.Signal transduction and targeted therapy · 2025Review
- Identification of immune and major depressive disorder-related diagnostic markers for early nonalcoholic fatty liver disease by WGCNA and machine learning.Frontiers in bioinformatics · 2025Article
- Article
- Current status and perspective on molecular targets and therapeutic intervention strategy in hepatic ischemia-reperfusion injury.Clinical and molecular hepatology · 2024Review
- Integrative analysis of the transcriptome and metabolome reveals the importance of hepatokine FGF21 in liver aging.Genes & diseases · 2024Article
- Neddylation inhibition prevents acetaminophen-induced liver damage by enhancing the anabolic cardiolipin pathway.Cell reports. Medicine · 2024Article
- TRIM26 deficiency enhancing liver regeneration through macrophage polarization and β-catenin pathway activation.Cell death & disease · 2024Article
- Transcriptional Profiling Underscores the Role of Preprocurement Allograft Metabolism and Innate Immune Status on Outcomes in Human Liver Transplantation.Annals of surgery open : perspectives of surgical history, education, and clinical approaches · 2024Article
Corrections and comments
- Erratum issuedErratum.2022
Authors and funding
37 authors at 15 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimsHepatic ischemia-reperfusion injury (IRI) is the leading cause of early posttransplantation organ failure as mitochondrial respiration and ATP production are affected. A shortage of donors has extended liver donor criteria, including aged or steatotic livers, which are more susceptible to IRI. Given the lack of an effective treatment and the extensive transplantation waitlist, we aimed at characterizing the effects of an accelerated mitochondrial activity by silencing methylation-controlled J protein (MCJ) in three preclinical models of IRI and liver regeneration, focusing on metabolically compromised animal models. APPROACH AND
resultsWild-type (WT), MCJ knockout (KO), and Mcj silenced WT mice were subjected to 70% partial hepatectomy (Phx), prolonged IRI, and 70% Phx with IRI. Old and young mice with metabolic syndrome were also subjected to these procedures. Expression of MCJ, an endogenous negative regulator of mitochondrial respiration, increases in preclinical models of Phx with or without vascular occlusion and in donor livers. Mice lacking MCJ initiate liver regeneration 12 h faster than WT and show reduced ischemic injury and increased survival. MCJ knockdown enables a mitochondrial adaptation that restores the bioenergetic supply for enhanced regeneration and prevents cell death after IRI. Mechanistically, increased ATP secretion facilitates the early activation of Kupffer cells and production of TNF, IL-6, and heparin-binding EGF, accelerating the priming phase and the progression through G
conclusionsBoosting mitochondrial activity by silencing MCJ could pave the way for a protective approach after major liver resection or IRI, especially in metabolically compromised, IRI-susceptible organs.
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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.