ArticleJournal of lipid research2022
Lipid droplet-mitochondria coupling via perilipin 5 augments respiratory capacity but is dispensable for FA oxidation.
Article in Journal of lipid research, 2022. 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, 63 citations in OpenAlex.
- 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
- Spatial architecture of immunometabolism: Mitochondrial‑organelle interfaces in immune signaling (Review).International journal of molecular medicine · 2026Review
- Loss of Rab8a-Dependent Tethering of Lipid Droplets to Mitochondria Contributes to Hypoxia-Reoxygenation Injury.MedComm · 2026Article
- The interplay of lipid droplets, mitochondria, and ER in governing hepatic lipid metabolism.Current opinion in cell biology · 2026Review
- PLIN5 Protects Against Ang II-Induced Podocyte Lipotoxicity by Interacting With FKBP8 and Preserving Lipid Droplet-Mitochondria Contact.Cell proliferation · 2026Article
- Compositional recalibrations of cardiolipin integrate loss of stearoyl-CoA desaturase 1 activity with mitochondrial decay in lipid-laden pancreatic β-cells.Cell communication and signaling : CCS · 2026Article
- Lipid droplets beyond storage: Cellular metabolic modulator in the diabetic heart (Review).International journal of molecular medicine · 2026Review
- Influence of PLIN5 and lipid composition on lipid droplet contact sites with other organelles.Biochemistry and biophysics reports · 2026Article
- Review
- Psoralidin, a main compound in Psoraleae Fructus, induces hepatotoxicity by impeding lipid oxidative catabolism and aggravating lipid accumulation in mice.Chinese medicine · 2026Article
- KIF13B Attenuates Sepsis-Induced Myocardial Dysfunction through the Stabilization of PLIN5.Research (Washington, D.C.) · 2026Article
- Acute deletion of PLIN5 in brown adipocytes causes mitochondrial dysfunction and cold intolerance.bioRxiv : the preprint server for biology · 2026Article
- Lipid droplet-mitochondria contact sites as druggable spatial-pharmacology targets in respiratory disease: cross-cell-type mechanisms and translational strategies.Frontiers in cell and developmental biology · 2026Review
- The inhibition mechanism ofFrontiers in microbiology · 2026Review
- Interactions between lipid droplets and mitochondria in metabolic diseases.Lipids in health and disease · 2025Review
- Perilipins: key targets for regulating lipid metabolism and alleviating abnormal lipid metabolism through exercise.Diabetology & metabolic syndrome · 2025Review
- Influence of diet-induced obesity and voluntary exercise training on cardiac lipids and mitochondrial function in mice.Journal of sport and health science · 2025Article
- Left ventricular myocardial molecular profile of human diabetic ischaemic cardiomyopathy.EMBO molecular medicine · 2025Article
- AMPK regulates ARF1 localization to membrane contact sites to facilitate fatty acid transfer between lipid droplets and mitochondria.Cell death & disease · 2025Article
- APOE4 reshapes the lipid droplet proteome and modulates microglial inflammatory responses.Neurobiology of disease · 2025Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Disturbances in lipid homeostasis can cause mitochondrial dysfunction and lipotoxicity. Perilipin 5 (PLIN5) decorates intracellular lipid droplets (LDs) in oxidative tissues and controls triacylglycerol (TG) turnover via its interactions with adipose triglyceride lipase and the adipose triglyceride lipase coactivator, comparative gene identification-58. Furthermore, PLIN5 anchors mitochondria to the LD membrane via the outermost part of the carboxyl terminus. However, the role of this LD-mitochondria coupling (LDMC) in cellular energy catabolism is less established. In this study, we investigated the impact of PLIN5-mediated LDMC in comparison to disrupted LDMC on cellular TG homeostasis, FA oxidation, mitochondrial respiration, and protein interaction. To do so, we established PLIN5 mutants deficient in LDMC whilst maintaining normal interactions with key lipolytic players. Radiotracer studies with cell lines stably overexpressing wild-type or truncated PLIN5 revealed that LDMC has no significant impact on FA esterification upon lipid loading or TG catabolism during stimulated lipolysis. Moreover, we demonstrated that LDMC exerts a minor if any role in mitochondrial FA oxidation. In contrast, LDMC significantly improved the mitochondrial respiratory capacity and metabolic flexibility of lipid-challenged cardiomyocytes, which was corroborated by LDMC-dependent interactions of PLIN5 with mitochondrial proteins involved in mitochondrial respiration, dynamics, and cristae organization. Taken together, this study suggests that PLIN5 preserves mitochondrial function by adjusting FA supply via the regulation of TG hydrolysis and that LDMC is a vital part of mitochondrial integrity.
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