ArticleJournal of lipid research2013
Cardiac-specific overexpression of perilipin 5 provokes severe cardiac steatosis via the formation of a lipolytic barrier.
Article in Journal of lipid research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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
70 citing papers in PubMed, 119 citations in OpenAlex.
- Lipid droplet dynamics and insulin sensitivity upon a 5-day high-fat diet in Caucasians and South Asians.Scientific reports · 2017Trial
- Bariatric surgery may alleviate MASLD by restoring mitochondria-lipid droplet structural and functional integrity through suppression of the Mitochondrial Fission Factor-Perilipin 5 axis.Molecular biomedicine · 2026Article
- Review
- Cardiac Lipid Metabolism: Cells, Metabolites, and Rhythms.Circulation research · 2026Review
- Lipid droplets beyond storage: Cellular metabolic modulator in the diabetic heart (Review).International journal of molecular medicine · 2026Review
- KIF13B Attenuates Sepsis-Induced Myocardial Dysfunction through the Stabilization of PLIN5.Research (Washington, D.C.) · 2026Article
- Transcriptional Response to Fasting Studied in the Liver of Mice That Express Phosphorylation Resistant Perilipin 5.Endocrinology · 2025Article
- Plin5: A potential therapeutic target for type 2 diabetes mellitus.Diabetology & metabolic syndrome · 2025Article
- Review
- Lipid droplets in central nervous system and functional profiles of brain cells containing lipid droplets in various diseases.Journal of neuroinflammation · 2025Review
- Omics Approaches to Study Perilipins and Their Significant Biological Role in Cardiometabolic Disorders.International journal of molecular sciences · 2025Review
- PLINs-mediated organelle interactions: a key of exercise-mediated improvement of skeletal muscle lipid metabolism disorders.Frontiers in endocrinology · 2025Review
- Mutational scanning pinpoints distinct binding sites of key ATGL regulators in lipolysis.Nature communications · 2024Article
- Lipotoxicity as a therapeutic target in obesity and diabetic cardiomyopathy.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2024Review
- Perilipin 5 deficiency aggravates cardiac hypertrophy by stimulating lactate production in leptin-deficient mice.Biology direct · 2023Article
- Cardiac lipid metabolism, mitochondrial function, and heart failure.Cardiovascular research · 2023Review
- Adverse cardiac remodeling augments adipose tissue ß-adrenergic signaling and lipolysis counteracting diet-induced obesity.The Journal of biological chemistry · 2023Article
- The Janus-Faced Role of Lipid Droplets in Aging: Insights from the Cellular Perspective.Biomolecules · 2023Review
- Hepatic PLIN5 Deficiency Impairs Lipogenesis through Mitochondrial Dysfunction.International journal of molecular sciences · 2022Article
- Review
10 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
Abstract
Cardiac triacylglycerol (TG) catabolism critically depends on the TG hydrolytic activity of adipose triglyceride lipase (ATGL). Perilipin 5 (Plin5) is expressed in cardiac muscle (CM) and has been shown to interact with ATGL and its coactivator comparative gene identification-58 (CGI-58). Furthermore, ectopic Plin5 expression increases cellular TG content and Plin5-deficient mice exhibit reduced cardiac TG levels. In this study we show that mice with cardiac muscle-specific overexpression of perilipin 5 (CM-Plin5) massively accumulate TG in CM, which is accompanied by moderately reduced fatty acid (FA) oxidizing gene expression levels. Cardiac lipid droplet (LD) preparations from CM of CM-Plin5 mice showed reduced ATGL- and hormone-sensitive lipase-mediated TG mobilization implying that Plin5 overexpression restricts cardiac lipolysis via the formation of a lipolytic barrier. To test this hypothesis, we analyzed TG hydrolytic activities in preparations of Plin5-, ATGL-, and CGI-58-transfected cells. In vitro ATGL-mediated TG hydrolysis of an artificial micellar TG substrate was not inhibited by the presence of Plin5, whereas Plin5-coated LDs were resistant toward ATGL-mediated TG catabolism. These findings strongly suggest that Plin5 functions as a lipolytic barrier to protect the cardiac TG pool from uncontrolled TG mobilization and the excessive release of free FAs.
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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.