ArticleOxidative medicine and cellular longevity2019
Plin5/p-Plin5 Guards Diabetic CMECs by Regulating FFAs Metabolism Bidirectionally.
Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Mechanism study of miR-324-3p driving myocardial infarction progression through regulation of myocardial inflammation.Journal of cardiothoracic surgery · 2026Article
- Plin5: A potential therapeutic target for type 2 diabetes mellitus.Diabetology & metabolic syndrome · 2025Article
- Plin5 inhibits proliferation and migration of vascular smooth muscle cell through interacting with PGC-1α following vascular injury.Bioengineered · 2022Article
- Plin5, a New Target in Diabetic Cardiomyopathy.Oxidative medicine and cellular longevity · 2022Review
- Traditional chinese medicine in coronary microvascular disease.Frontiers in pharmacology · 2022Review
- [Effect of dissipating phlegm and blood stasis simultaneously on AGEs/RAGE axis and oxidative stress in rats with diabetic myocardial microangiopathy].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021Article
- Perilipin 5 is a novel target of nuclear receptor LRH-1 to regulate hepatic triglycerides metabolism.BMB reports · 2021Article
- Research progress on the molecular mechanism of coronary microvascular endothelial cell dysfunction.International journal of cardiology. Heart & vasculature · 2021Review
- The biology of lipid droplet-bound mitochondria.Seminars in cell & developmental biology · 2020Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHyper-free fatty acidemia (HFFA) impairs cardiac capillaries, as well as type 2 diabetes mellitus (T2DM). Perilipin 5 (Plin5) maintains metabolic balance of free fatty acids (FFAs) in high oxidative tissues via the states of nonphosphorylation and phosphorylation. However, when facing to T2DM-HFFA, Plin5's role in cardiac microvascular endothelial cells (CMECs) is not defined.
methodsIn mice of WT or Plin5
resultsIn CMECs, HFFAs aggravated cell injury induced by HG and activated Plin5 expression. In mice with T2DM-HFFA, Plin5 deficiency reduced number of cardiac capillaries, worsened structural incompleteness, and enhanced diastolic dysfunction. Moreover, in CMECs treated with HG-HFFAs, both ablation and phosphorylation of Plin5 reduced LDs content, increased intracellular FFAs, stimulated mitochondrial
conclusionPlin5 preserves lipid balance and cell survival in diabetic CMECs by regulating FFAs metabolism bidirectionally via the states of nonphosphorylation and phosphorylation.
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