Ask about this productRelated genes to: ATGL antibody
- Gene:
- PNPLA2 NIH gene
- Name:
- patatin like phospholipase domain containing 2
- Previous symbol:
- -
- Synonyms:
- desnutrin, TTS-2.2, ATGL, FP17548, iPLA2zeta
- Chromosome:
- 11p15.5
- Locus Type:
- gene with protein product
- Date approved:
- 2004-09-06
- Date modifiied:
- 2015-11-23
Related products to: ATGL antibody
Related articles to: ATGL antibody
- Although metabolic dysregulation serves as a pivotal hallmark in glioma, the detailed information about the lipid metabolism regulation is largely unknown. In the context of this investigation, we have identified B7-H3 - an immune checkpoint molecule of the B7 family - as a regulator of lipid metabolism in glioma. - Source: PubMed
Publication date: 2026/05/07
Hu XiaohanZhang LiuqingLi YuepengWang JianweiQi WanqingAn JingnanLi XiaoweiYang YuanWeng ZhenLi FangXu Yunyun - Perivascular adipose tissue (PVAT) surrounds most peripheral blood vessels and exerts an anti-contractile influence through paracrine mediators. Although numerous vasoactive factors have been identified, the mechanisms linking adipocyte metabolism to PVAT-dependent modulation of vascular tone remain poorly defined. Because adipocytes store energy as triglycerides hydrolyzed by adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) to generate free fatty acids, we hypothesized that lipolysis-derived fatty acids may contribute to PVAT's anti-contractile actions through activation of long-chain fatty acid-sensing G protein-coupled receptors, Gpr40 and/or Gpr120. - Source: PubMed
Hyatt MirandaRodrigues Dos Passos RinaldoAraujo Fenix AWilson Emily WWaigi Emily WCosta Tiago JSilva Darízy FWebb R ClintonWenceslau Camilla FMcCarthy Cameron G - Acute kidney injury (AKI) is a clinically significant syndrome characterized by a rapid decline in renal function, affecting over 50% of patients in intensive care units. Ferroptosis, a recently identified form of regulated cell death, is driven by iron-dependent lipid peroxidation and has been implicated in AKI pathogenesis. Emerging evidence suggests that lipophagy - a selective autophagic degradation of lipid droplets - potentiates ferroptosis, though the upstream regulatory mechanisms remain poorly understood. ESRRA (estrogen related receptor, alpha), a key transcriptional regulator of fatty acid metabolism and macroautophagy/autophagy, may play a critical role in this process. In this study, we identified ESRRA as a pivotal transcription factor in proximal tubular epithelial cells using single-cell transcriptomic analysis. To investigate its functional role, we employed wild-type mice and tubular epithelial cell-specific deficient mice to establish AKI models. Our findings demonstrated that ESRRA exerted a protective effect by modulating the RAB7-dependent lipophagy-ferroptosis axis. Furthermore, integrating chromatin Immunoprecipitation (ChIP)-seq and JASPAR database analyses, we predicted as a direct transcriptional target of ESRRA. Mechanistically, ESRRA bind to a specific promoter region within , enhancing its expression and subsequently activating the AKT-MTOR signaling pathway, which is required for the suppression of RAB7 mediated lipophagy in renal tubular epithelial cells, thereby attenuating AKI progression. ACSL4: acyl-CoA synthetase long-chain family member 4; AKI: acute kidney injury; AKT/PKB: Akt serine/threonine kinase; ChIP: chromatin Immunoprecipitation; Cis-AKI: cisplatin-induced acute kidney injury; CI-AKI: contrast-induced acute kidney injury; ER: endoplasmic reticulum; ESRRA: estrogen related receptor, alpha; FFAs: free fatty acids; FA-AKI: folic acids-induced acute kidney injury; GPX4: glutathione peroxidase 4; GSH: glutathione; HK-2 cells: human renal proximal tubular epithelial cells; LDs: lipid droplets; LV: lentivirus; MAP1LC3B/LC3B: microtubule-associated protein 1 light chain 3 beta; MTOR: mechanistic target of rapamycin kinase; PPARGC1A/PGC1-α: PPARG coactivator 1 alpha; PIK3CA: phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha; PLIN2: perilipin 2; PNPLA2/ATGL: patatin-like phospholipase domain containing 2; PT: proximal tubular epithelial cells; PUFA: polyunsaturated fatty acid; RAB7: RAB7, member RAS oncogene family; ROS: reactive oxygen species; SQSTM1: sequestosome 1. - Source: PubMed
Publication date: 2026/05/05
Yang YuantingZhu XuyingFang YanLi JialinShao XinghuaLi ShuJin HaijiaoQi ChaojunLi ZhenyuanGu LeyiMou ShanLin QishengNi Zhaohui - Triglyceride (TG) deposit cardiomyovasculopathy (TGCV) was first identified in Japanese patients with homozygous mutations in PNPLA2 encoding adipose triglyceride lipase. TGs and fatty acids released by lipolytic action are major energy substrates in a normal heart. In TGCV, the defective intracellular lipolysis of long-chain TGs causes cellular steatosis and energy failure mainly in cardiomyocytes and vascular smooth muscle cells. One of the major characteristics is diffuse narrowing TG-deposited coronary atherosclerosis which is distinct from classic cholesterol-induced focal lesions. TGCV comprises primary and idiopathic subtypes with and without homozygous PNPLA2 mutations, respectively. Genetic causes or backgrounds of idiopathic TGCV (I-TGCV) remain undetermined. We established the diagnostic criteria without requirement of genetic tests, including the reduced washout rate (<10%) of iodine-123-β-methyl-p-iodophenyl-pentadecanoic acid in myocardial single-photon emission computed tomography, which reflects defective lipolysis, as an essential item. Serum TG level and body mass index are irrelevant to the diagnosis. As of October 2024, 15 primary TGCV (P-TGCV) and 976 I-TGCV cases were diagnosed across all Japanese prefectures. The cardiac symptoms of P-TGCV and I-TGCV occurred in patients aged in their 30s and 50s, respectively. The patients exhibited heart failure (HF), diffuse coronary artery disease including vasospastic angina, and ventricular arrhythmia. The prognosis was very severe in patients with P-TGCV manifesting HF with reduced ejection fraction unless receiving cardiac transplantation. In I-TGCV, the 5-year-overall and cardiovascular event-free survival rates were 71.8% and 54.0%, respectively, with standard remedies. Tricaprin/trisdecanoin, a medium-chain TG that facilitates myocardial lipolysis, is being developed as a first-in-class orphan drug for TGCV. TGCV is a novel class of adult-onset cardiovascular disease caused by the defective lipolysis of long-chain TGs. Many patients with TGCV exhibiting high cardiovascular risk remain undiagnosed; thus, increased awareness of this emerging disease is required among cardiologists of all subspecialties. - Source: PubMed
Publication date: 2026/04/13
Mori TatsuyaHirano Ken-IchiMiyauchi HideyukiIkeda YoshihikoHigashi MasahiroNakano YusukeKanda TakahiroNagasawa YasuyukiInaba TohruOkumura TakahiroZaima NobuhiroKobayashi KunihisaMatsumoto NaoyaYamada TomomiAmano TetsuyaFujimoto Shinichiro - Bone formation requires a substantial energy supply to sustain extracellular matrix production and mineralization, yet the temporal contribution of lipid metabolism during osteoblast maturation remains incompletely characterized. This study investigated the molecular and transcriptional remodeling of lipid metabolism. Intracellular lipid distribution was analyzed by confocal microscopy using Nile Red staining. Transcriptional modulation of lipid synthesis, storage, lipolysis, genes associated with mitochondrial fatty acid oxidation, and osteogenic markers were assessed by quantitative real-time PCR, and the biochemical composition was evaluated by Raman spectroscopy. Early stages of spheroid development showed higher expression of genes involved in lipid synthesis and storage (FASN, DGAT2, and PLIN2) together with intracellular lipid accumulation, whereas later stages displayed increased expression of lipolytic and β-oxidation markers (PNPLA2/ATGL, CPT1A, and HADHA), accompanied by the redistribution of lipid droplets. The Raman analysis revealed a time-dependent variation of lipid-associated CH/CH bands and modulation of protein-related Amide I-III signals, consistent with biochemical remodeling during maturation. Overall, the data indicate a coordinated transcriptional shift from lipid accumulation-associated pathways toward lipid mobilization during osteogenic progression in a 3D culture. This model provides a controlled experimental platform for investigating metabolic regulation during bone formation and for studying metabolic alterations associated with skeletal disorders. - Source: PubMed
Publication date: 2026/04/07
Rizzo Maria GiovannaMorganti DarioSciuto Emanuele LuigiSmeriglio AntonellaCannatà GiorgiaFazio BarbaraGuglielmino Salvatore P PTrombetta DomenicoFaggio CaterinaConoci Sabrina