ArticleScientific reports2017
Plin5 alleviates myocardial ischaemia/reperfusion injury by reducing oxidative stress through inhibiting the lipolysis of lipid droplets.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 80 citations in OpenAlex.
- Lipid droplets as redox-active organelles after spinal cord injury: lipid peroxidation, mitochondrial dysfunction, and neuroinflammation.Redox report : communications in free radical research · 2026Review
- Lipid droplet-associated proteins: Roles in cardiovascular diseases.Journal of lipid research · 2026Review
- Review
- Effect of blood lipid on myocardial injury in rats with myocardial infarction.American journal of translational research · 2026Article
- Interactions between lipid droplets and mitochondria in metabolic diseases.Lipids in health and disease · 2025Review
- Mitochondria and myocardial ischemia/reperfusion injury: Effects of Chinese herbal medicine and the underlying mechanisms.Journal of pharmaceutical analysis · 2025Review
- The Lipid-Oxidative Stress Axis: Novel Therapeutic Targets for Podocytopathy.Journal of inflammation research · 2025Review
- Perilipin 5 alleviates ferroptosis of cardiomyocytes by targeting USP10-p53-TfR proteasome-dependent degradation.Frontiers in medicine · 2025Article
- The role of Perilipin 5 in pathological myocardial remodeling.Frontiers in pharmacology · 2025Review
- PLINs-mediated organelle interactions: a key of exercise-mediated improvement of skeletal muscle lipid metabolism disorders.Frontiers in endocrinology · 2025Review
- Roles of lipid droplets and related proteins in metabolic diseases.Lipids in health and disease · 2024Review
- Lipid droplets and fatty acid-induced lipotoxicity: in a nutshell.FEBS letters · 2024Article
- Role of Perilipins in Oxidative Stress-Implications for Cardiovascular Disease.Antioxidants (Basel, Switzerland) · 2024Review
- Mitochondria isolated from lipid droplets of white adipose tissue reveal functional differences based on lipid droplet size.Life science alliance · 2024Article
- Molecular mechanisms of lipid droplets-mitochondria coupling in obesity and metabolic syndrome: insights and pharmacological implications.Frontiers in physiology · 2024Review
- Oxidative stress mediates the inhibitory effects of Manzamine A on uterine leiomyoma cell proliferation and extracellular matrix deposition via SOAT inhibition.Redox biology · 2023Article
- 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
- Challenges in Pharmacological Intervention in Perilipins (PLINs) to Modulate Lipid Droplet Dynamics in Obesity and Cancer.Cancers · 2023Review
- PLIN5 interacts with FATP4 at membrane contact sites to promote lipid droplet-to-mitochondria fatty acid transport.Developmental cell · 2023Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial ischaemia-reperfusion (I/R) injury is a complex pathophysiological process. Current research has suggested that energy metabolism disorders, of which the abnormal consumption of fatty acids is closely related, compose the main pathological basis for myocardial I/R injury. Lipid droplets (LD) are critical regulators of lipid metabolism by LD-associated proteins. Among the lipid droplet proteins, the perilipin family members regulate lipolysis and lipogenesis through different mechanisms. Plin5, an important perilipin protein, promotes LD generation and lowers fatty acid oxidation, thus protecting the myocardium from lipotoxicity. This study investigated the protective effects of Plin5 in I/R myocardium. Our results indicated that Plin5 deficiency exacerbated the myocardial infarct area, aggravated left ventricular systolic dysfunction, reduced lipid storage, and elevated free fatty acids. Plin5-deficient myocardium exhibited severely damaged mitochondria, elevated reactive oxygen species (ROS) and malondialdehyde (MDA) levels, and decreased superoxide dismutase (SOD) activity. Furthermore, the decreased phosphorylation of PI3K/Akt in Plin5-null cardiomyocytes might contribute to I/R injury aggravation. In conclusion, Plin5, a new regulator of myocardial lipid metabolism, decreases free fatty acid peroxidation by inhibiting the lipolysis of intracellular lipid droplets, thus providing cardioprotection against I/R injury and shedding new light on therapeutic solutions for I/R diseases.
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