ArticleThe Journal of biological chemistry2013
Functional cardiac lipolysis in mice critically depends on comparative gene identification-58.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 64 citations in OpenAlex.
- Lipid droplets beyond storage: Cellular metabolic modulator in the diabetic heart (Review).International journal of molecular medicine · 2026Review
- Lipid droplets as cell fate determinants in skeletal muscle.Trends in endocrinology and metabolism: TEM · 2025Review
- Adverse cardiac remodeling augments adipose tissue ß-adrenergic signaling and lipolysis counteracting diet-induced obesity.The Journal of biological chemistry · 2023Article
- Review
- Article
- Protective Effects of Tiaoganquzhi Decoction in Treating inflammatory Injury of Nonalcoholic Fatty liver Disease by Promoting CGI-58 and Inhibiting Expression of NLRP3 Inflammasome.Frontiers in pharmacology · 2022Article
- Cardiac-specific CGI-58 deficiency activates the ER stress pathway to promote heart failure in mice.Cell death & disease · 2021Article
- Mitochondria in skin health, aging, and disease.Cell death & disease · 2020Review
- The Role of Adipose Triglyceride Lipase and Cytosolic Lipolysis in Cardiac Function and Heart Failure.Cell reports. Medicine · 2020Review
- Low cardiac lipolysis reduces mitochondrial fission and prevents lipotoxic heart dysfunction in Perilipin 5 mutant mice.Cardiovascular research · 2020Article
- CGI-58: Versatile Regulator of Intracellular Lipid Droplet Homeostasis.Advances in experimental medicine and biology · 2020Review
- The lipid droplet-associated protein ABHD5 protects the heart through proteolysis of HDAC4.Nature metabolism · 2019Article
- Article
- The α/β-hydrolase domain-containing 4- and 5-related phospholipase Pummelig controls energy storage inJournal of lipid research · 2019Article
- Of mice and men: The physiological role of adipose triglyceride lipase (ATGL).Biochimica et biophysica acta. Molecular and cell biology of lipids · 2019Review
- N-acetylaspartate pathway is nutrient responsive and coordinates lipid and energy metabolism in brown adipocytes.Biochimica et biophysica acta. Molecular cell research · 2019Article
- Manifestations and mechanisms of myocardial lipotoxicity in obesity.Journal of internal medicine · 2018Review
- Adipose tissue ATGL modifies the cardiac lipidome in pressure-overload-induced left ventricular failure.PLoS genetics · 2018Article
- Novel Pharmacological Probes Reveal ABHD5 as a Locus of Lipolysis Control in White and Brown Adipocytes.The Journal of pharmacology and experimental therapeutics · 2017Article
- Critical roles for α/β hydrolase domain 5 (ABHD5)/comparative gene identification-58 (CGI-58) at the lipid droplet interface and beyond.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2017Review
Corrections and comments
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Authors and funding
17 authors at 2 institutions in 1 country.
Funding
Abstract
Efficient catabolism of cellular triacylglycerol (TG) stores requires the TG hydrolytic activity of adipose triglyceride lipase (ATGL). The presence of comparative gene identification-58 (CGI-58) strongly increased ATGL-mediated TG catabolism in cell culture experiments. Mutations in the genes coding for ATGL or CGI-58 in humans cause neutral lipid storage disease characterized by TG accumulation in multiple tissues. ATGL gene mutations cause a severe phenotype especially in cardiac muscle leading to cardiomyopathy that can be lethal. In contrast, CGI-58 gene mutations provoke severe ichthyosis and hepatosteatosis in humans and mice, whereas the role of CGI-58 in muscle energy metabolism is less understood. Here we show that mice lacking CGI-58 exclusively in muscle (CGI-58KOM) developed severe cardiac steatosis and cardiomyopathy linked to impaired TG catabolism and mitochondrial fatty acid oxidation. The marked increase in ATGL protein levels in cardiac muscle of CGI-58KOM mice was unable to compensate the lack of CGI-58. The addition of recombinant CGI-58 to cardiac lysates of CGI-58KOM mice completely reconstituted TG hydrolytic activities. In skeletal muscle, the lack of CGI-58 similarly provoked TG accumulation. The addition of recombinant CGI-58 increased TG hydrolytic activities in control and CGI-58KOM tissue lysates, elucidating the limiting role of CGI-58 in skeletal muscle TG catabolism. Finally, muscle CGI-58 deficiency affected whole body energy homeostasis, which is caused by impaired muscle TG catabolism and increased cardiac glucose uptake. In summary, this study demonstrates that functional muscle lipolysis depends on both CGI-58 and ATGL.
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Registered trials
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