ArticleCell metabolism2025
Human genetics identify convergent signals in mitochondrial LACTB-mediated lipid metabolism in cardiovascular-kidney-metabolic syndrome.
Article in Cell metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Cardiovascular-kidney-metabolic syndrome as a mitochondrial systems disorder.Nature reviews. Nephrology · 2026Review
- Cuproptosis and ferroptosis: signal pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Biomarkers and Risk Prediction in Cardiovascular-Kidney-Metabolic Syndrome: A Comprehensive Review.Reviews in cardiovascular medicine · 2026Review
- Silencing arachidonate 15-lipoxygenase alleviates hypoxia-induced cognitive impairment through the mediation of phospholipase A2 group IVC-LPC18:0 to suppress ferroptosis.Molecular biomedicine · 2026Article
- Multi-omics-driven precision medicine.iMeta · 2026Review
- Metainflammation, Mitochondrial Dysfunction, and Organokine Crosstalk: A Central Axis Linking Metabolic Syndrome to Cardiovascular Diseases.International journal of molecular sciences · 2026Review
- Mitochondrial Dysfunction at the Intersection of CKM Syndrome: Molecular Mechanisms and Path-to-Target Therapies.International journal of molecular sciences · 2026Review
- Cardiovascular-kidney-metabolic syndrome: a comprehensive review of pathophysiology, epidemiology, diagnosis, and management.Cardiovascular diabetology · 2026Review
- Emerging multidimensional biomarker system for cardiovascular-kidney-metabolic syndrome: from multi-omics integration to clinical artificial intelligence.Cardiovascular diabetology · 2026Review
- Fiber type-specific expression of LACTB leverages a function in oxidative metabolism.Histochemistry and cell biology · 2026Article
- Genomic Structural Equation Modeling Reveals Cardiovascular-Kidney-Metabolic Syndrome Genetic Architecture.Journal of diabetes · 2026Article
- The depletion of serine beta-lactamase-like protein (LACTB) ameliorates metabolic dysfunction-associated steatotic liver disease by reducing ubiquitin-mediated degradation of carnitine palmitoyltransferase 2.Diabetes, obesity & metabolism · 2026Article
- Editorial: Cardiovascular-kidney-metabolic syndrome: interorgan crosstalk, pathophysiology, and therapeutics.Frontiers in physiology · 2026Article
- Interpretable bioimpedance-based modeling of body composition and metabolic indices related to physical function in maintenance hemodialysis patients.Frontiers in nutrition · 2026Article
- Bioenergetics and lipid metabolism in Alzheimer's disease: From cell biology to systemic health.Journal of internal medicine · 2026Review
- The tumor suppressor LACTB remodels mitochondria to promote cytochrome c release and apoptosis.Science advances · 2025Article
- The Ferroptosis-Mitochondrial Axis in Depression: Unraveling the Feedforward Loop of Oxidative Stress, Metabolic Homeostasis Dysregulation, and Neuroinflammation.Antioxidants (Basel, Switzerland) · 2025Review
- Prioritization of Lipid Metabolism Targets for the Diagnosis and Treatment of Cardiovascular Diseases.Research (Washington, D.C.) · 2025Article
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Authors and funding
17 authors.
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Abstract
The understanding of cardiovascular-kidney-metabolic syndrome remains difficult despite recently performed large scale genome-wide association studies. Here, we identified beta-lactamase (LACTB), a novel gene whose expression is targeted by genetic variations causing kidney dysfunction and hyperlipidemia. Mice with LACTB deletion developed impaired glucose tolerance, elevated lipid levels, and increased sensitivity to kidney disease, while mice with tubule-specific overexpression of LACTB were protected from kidney injury. We show that LACTB is a novel mitochondrial protease cleaving and activating phospholipase A2 group VI (PLA2G6), a kidney-metabolic risk gene itself. Genetic deletion of PLA2G6 in tubule-specific LACTB-overexpressing mice abolished the protective function of LACTB. Via mouse and human lipidomic studies, we show that LACTB and downstream PLA2G6 convert oxidized phosphatidylethanolamine to lyso-phosphatidylethanolamine and thereby regulate mitochondrial function and ferroptosis. In summary, we identify a novel gene and a core targetable pathway for kidney-metabolic disorders.
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