ArticleNature communications2024
Mic19 depletion impairs endoplasmic reticulum-mitochondrial contacts and mitochondrial lipid metabolism and triggers liver disease.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed.
- MIC13-linked cristae disruption causes metabolic failure and early fibrotic remodelling in mitochondrial liver disease.Cell death & disease · 2026Article
- RcAlb-PepII Perturbs the Proteomic Profile ofMicroorganisms · 2026Article
- Zfp217 Regulates Hepatic de Novo Lipogenesis via METTL3-Mediated N6-Methyladenosine Modification of SREBF1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Lipidomics Based on HILIC-ESI-HRMS Reveal Subtle Changes in the Mitochondrial Phospholipidome of Mouse Embryonic Fibroblasts Expressing Pathogenic Variants of Human OPA1 Protein.Molecules (Basel, Switzerland) · 2026Article
- Organelle-specific fluorescent probes for live imaging at the nanoscale.Science China. Life sciences · 2026Review
- Mitochondria‑endoplasmic reticulum contact site nexus: Molecular integration, disease pathogenesis and therapeutic opportunities (Review).International journal of molecular medicine · 2026Review
- Mitochondrial quality control in health and disease: mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Mitochondrial Communication with Cellular Organelles in the Pathogenesis of Fatty Liver Disease in Domestic and Model Animals.Animals : an open access journal from MDPI · 2026Review
- Acute hypoxia induces liver mitochondrial and endoplasmic reticulum stress in adult grass carp (Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2026Article
- Bufalin Suppresses Pancreatic Ductal Adenocarcinoma Through ER Stress-Ferroptosis Crosstalk Associated with IPInternational journal of molecular sciences · 2026Article
- Research progress on the roles and mechanisms of flavonoid monomers in liver diseases: a review.Molecular biology reports · 2026Review
- A dynamic gateway: Uncovering the expanded human TOM complex interactome and its regulatory complexity.Science advances · 2026Article
- The MICOS Complex Regulates Mitochondrial Structure and Oxidative Stress During Age-Dependent Structural Deficits in the Kidney.Aging cell · 2026Article
- Metabolic adaptation to IMMT deficiency through the ATF6-PPARγ axis is contingent on TP53 mutation status in breast cancer.Cell death & disease · 2026Article
- Alzheimer's disease: disrupted communication between the endoplasmic reticulum and mitochondria.Journal of neurology · 2026Review
- Dynamic collaboration between mitochondria and organelles: mechanisms, functions, and disease implications.Apoptosis : an international journal on programmed cell death · 2026Review
- Spatiotemporal Ca2+ nanodomain remodeling at MERCS regulates mitochondrial proteostasis.Protein & cell · 2026Article
- Mitochondrial interplay with membrane organelles in health and disease.Cell communication and signaling : CCS · 2026Review
- The spatiotemporal dynamics of MAMs: mechanisms, pathologies, and therapeutic rewiring.Cellular & molecular biology letters · 2026Review
- The MICOS Complex Regulates Mitochondrial Structure and Oxidative Stress During Age-Dependent Structural Deficits in the Kidney.bioRxiv : the preprint server for biology · 2026Article
6 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors.
Funding
Abstract
Endoplasmic reticulum (ER)-mitochondria contacts are critical for the regulation of lipid transport, synthesis, and metabolism. However, the molecular mechanism and physiological function of endoplasmic reticulum-mitochondrial contacts remain unclear. Here, we show that Mic19, a key subunit of MICOS (mitochondrial contact site and cristae organizing system) complex, regulates ER-mitochondria contacts by the EMC2-SLC25A46-Mic19 axis. Mic19 liver specific knockout (LKO) leads to the reduction of ER-mitochondrial contacts, mitochondrial lipid metabolism disorder, disorganization of mitochondrial cristae and mitochondrial unfolded protein stress response in mouse hepatocytes, impairing liver mitochondrial fatty acid β-oxidation and lipid metabolism, which may spontaneously trigger nonalcoholic steatohepatitis (NASH) and liver fibrosis in mice. Whereas, the re-expression of Mic19 in Mic19 LKO hepatocytes blocks the development of liver disease in mice. In addition, Mic19 overexpression suppresses MCD-induced fatty liver disease. Thus, our findings uncover the EMC2-SLC25A46-Mic19 axis as a pathway regulating ER-mitochondria contacts, and reveal that impairment of ER-mitochondria contacts may be a mechanism associated with the development of NASH and liver fibrosis.
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