ArticleNature communications2022
Adipocyte lysoplasmalogenase TMEM86A regulates plasmalogen homeostasis and protein kinase A-dependent energy metabolism.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- Emerging complexities of phospholipid metabolism in adipose tissue.Molecules and cells · 2026Review
- PLA2G2F/lysoplasmalogen axis links epidermal lipid metabolism to type 2 inflammation and itch in atopic dermatitis.Frontiers in immunology · 2026Article
- TMEM120A maintains adipose tissue lipid homeostasis through ER CoA channeling.Nature communications · 2025Article
- Comparative analysis of LJ-4378 and tirzepatide in mouse models of obesity and weight regain.Archives of pharmacal research · 2025Article
- The Changes in Plasmalogens: Chemical Diversity and Nutritional Implications-A Narrative Review.Nutrients · 2025Review
- Comparative Analyses of Gene and Protein Expressions and the Lipid Contents in Intramuscular and Subcutaneous Fat Tissues in Fattening Steers.Animals : an open access journal from MDPI · 2025Article
- SPNS1 variants cause multiorgan disease and implicate lysophospholipid transport as critical for mTOR-regulated lipid homeostasis.The Journal of clinical investigation · 2025Article
- BNIP3-mediated mitophagy in macrophages regulates obesity-induced adipose tissue metaflammation.Autophagy · 2025Article
- Alterations in ether lipid metabolism in obesity revealed by systems genomics of multi-omics datasets.PLoS biology · 2025Article
- Unraveling the complexities of diet induced obesity and glucolipid dysfunction in metabolic syndrome.Diabetology & metabolic syndrome · 2025Review
- Modulation of endogenous plasmalogens by genetic ablation of lysoplasmalogenase (Tmem86b) in mice.Journal of lipid research · 2025Article
- Integrated Multi-Tissue Lipidomics and Transcriptomics Reveal Differences in Lipid Composition Between Mashen and Duroc × (Landrace × Yorkshire) Pigs.Animals : an open access journal from MDPI · 2025Article
- An innovative approach using CRISPR-ribonucleoprotein packaged in virus-like particles to generate genetically engineered mouse models.Nature communications · 2025Article
- Application of Liquid Chromatography/Tandem Mass Spectrometry for Quantitative Analysis of Plasmalogens in Preadolescent Children-The Hokkaido Study.Diagnostics (Basel, Switzerland) · 2025Article
- Review
- TM4SF19-mediated control of lysosomal activity in macrophages contributes to obesity-induced inflammation and metabolic dysfunction.Nature communications · 2024Article
- Dietary "Beigeing" Fat Contains More Phosphatidylserine and Enhances Mitochondrial Function while Counteracting Obesity.Research (Washington, D.C.) · 2024Article
- Genome-wide loss-of-function screen using human pluripotent stem cells to study virus-host interactions for SARS-CoV-2.Stem cell reports · 2023Article
- Lipid remodeling of adipose tissue in metabolic health and disease.Experimental & molecular medicine · 2023Review
- Article
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 3 countries.
Funding
Abstract
Dysregulation of adipose tissue plasmalogen metabolism is associated with obesity-related metabolic diseases. We report that feeding mice a high-fat diet reduces adipose tissue lysoplasmalogen levels and increases transmembrane protein 86 A (TMEM86A), a putative lysoplasmalogenase. Untargeted lipidomic analysis demonstrates that adipocyte-specific TMEM86A-knockout (AKO) increases lysoplasmalogen content in adipose tissue, including plasmenyl lysophosphatidylethanolamine 18:0 (LPE P-18:0). Surprisingly, TMEM86A AKO increases protein kinase A signalling pathways owing to inhibition of phosphodiesterase 3B and elevation of cyclic adenosine monophosphate. TMEM86A AKO upregulates mitochondrial oxidative metabolism, elevates energy expenditure, and protects mice from metabolic dysfunction induced by high-fat feeding. Importantly, the effects of TMEM86A AKO are largely reproduced in vitro and in vivo by LPE P-18:0 supplementation. LPE P-18:0 levels are significantly lower in adipose tissue of human patients with obesity, suggesting that TMEM86A inhibition or lysoplasmalogen supplementation might be therapeutic approaches for preventing or treating obesity-related metabolic diseases.
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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.