ArticleCell metabolism2010
Cardiolipin remodeling by ALCAT1 links oxidative stress and mitochondrial dysfunction to obesity.
Article in Cell metabolism, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02230839 (Muscle Insulin Resistance In Aging), which is not on this map. Cited by 166 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Muscle Insulin Resistance In Aging
Who cites it
166 citing papers in PubMed, 291 citations in OpenAlex.
- Mitochondrial membrane lipid cardiolipin controls fiber-type adaptations in aging muscle via estrogen-related receptor γ.Nature aging · 2026Article
- Role of mitochondria-associated ER membranes in lipid metabolism: implications for renal lipotoxicity.Bioscience reports · 2026Review
- Omega-3 fatty acid supplementation improves skeletal muscle mitochondrial function in a model of Barth syndrome.JCI insight · 2026Article
- Mitochondrial quality control in human ageing and longevity.Nature metabolism · 2026Review
- Compositional recalibrations of cardiolipin integrate loss of stearoyl-CoA desaturase 1 activity with mitochondrial decay in lipid-laden pancreatic β-cells.Cell communication and signaling : CCS · 2026Article
- ALCAT1 promotes diabetic cardiomyopathy by linking myocardial tetralinoleoyl cardiolipin deficiency to lipotoxicity.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- CTPS1 modulates mitophagy to propel diffuse large B-cell lymphoma via reshaping CEPT1-mediated phospholipid metabolism.Redox biology · 2026Article
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- LPLAT11/MBOAT7-driven phosphatidylinositol remodeling ensures radial glial cell integrity in developing neocortex.iScience · 2026Article
- Complex I Modulator BI4500 Reduces MASH by Limiting Oxidative Stress and Reprogramming Lipid Metabolism via AMPK in MCD Rats.Antioxidants (Basel, Switzerland) · 2026Article
- Review
- Advances in the Rational Design, Mechanisms, and Applications of Lanthanide Nanoparticles for the Regulation of Reactive Oxygen Species.International journal of nanomedicine · 2026Review
- Advances in Cardiolipin Analysis: Applications in Central Nervous System Disorders and Nutrition Interventions.Biomolecules · 2026Review
- Altered mitochondrial functionality in metabolic disorders: insights fromFrontiers in endocrinology · 2026Review
- Influence of diet-induced obesity and voluntary exercise training on cardiac lipids and mitochondrial function in mice.Journal of sport and health science · 2025Article
- Transcriptomic Analysis Reveals Regulatory Responses of Fatty Acid Positional Distribution in Triacylglycerols and Lipid Composition to Dietary n-3 HUFA in the Muscle ofAnimals : an open access journal from MDPI · 2025Article
- Identification of lipid metabolism-related genes in myocardial infarction: implications for diagnosis and therapy.Journal of cardiothoracic surgery · 2025Article
- Lipid metabolism in health and disease: Mechanistic and therapeutic insights for Parkinson's disease.Chinese medical journal · 2025Review
- Aerobic Exercise Alleviates Cardiac Dysfunction Correlated with Lipidomics and Mitochondrial Quality Control.Antioxidants (Basel, Switzerland) · 2025Article
- Diet-induced obesity dampens the temporal oscillation of hepatic mitochondrial lipids.Journal of lipid research · 2025Article
106 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
Abstract
Oxidative stress causes mitochondrial dysfunction and metabolic complications through unknown mechanisms. Cardiolipin (CL) is a key mitochondrial phospholipid required for oxidative phosphorylation. Oxidative damage to CL from pathological remodeling is implicated in the etiology of mitochondrial dysfunction commonly associated with diabetes, obesity, and other metabolic diseases. Here, we show that ALCAT1, a lyso-CL acyltransferase upregulated by oxidative stress and diet-induced obesity (DIO), catalyzes the synthesis of CL species that are highly sensitive to oxidative damage, leading to mitochondrial dysfunction, ROS production, and insulin resistance. These metabolic disorders were reminiscent of those observed in type 2 diabetes and were reversed by rosiglitazone treatment. Consequently, ALCAT1 deficiency prevented the onset of DIO and significantly improved mitochondrial complex I activity, lipid oxidation, and insulin signaling in ALCAT1(-/-) mice. Collectively, these findings identify a key role of ALCAT1 in regulating CL remodeling, mitochondrial dysfunction, and susceptibility to DIO.
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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.