Ask about this productRelated genes to: PPARA antibody
- Gene:
- PPARA NIH gene
- Name:
- peroxisome proliferator activated receptor alpha
- Previous symbol:
- PPAR
- Synonyms:
- hPPAR, NR1C1
- Chromosome:
- 22q13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-01
- Date modifiied:
- 2016-10-05
Related products to: PPARA antibody
Related articles to: PPARA antibody
- Mitochondrial DNA (mtDNA) polymorphisms have been associated with production traits in farm animals, including backfat thickness in pigs, yet direct in vivo evidence establishing a causal link between specific mtDNA haplotypes and fat deposition remains limited. In this study, we generated transmitochondrial pigs (mitopigs) by combining the Dapulian nuclear genome with Wuzhishan mtDNA via somatic cell nuclear transfer, introducing 23 mtDNA mutations relative to controls. Mitopigs exhibited significantly increased backfat thickness at 5 months, a difference that persisted in their offspring, without significant differences in body weight, body size, or litter size. Fibroblasts derived from mitopigs exhibited reduced mtDNA copy numbers, decreased expression of mitochondrial biogenesis genes (PPARA, PPARGC1A, RRM2B, and LRPPRC), impaired mitochondrial respiration, elevated reactive oxygen species (ROS), and upregulated adipogenic transcription factors (CEBPA, CEBPB, and PPARG). Consistent with these fibroblast findings, backfat tissue of mitopigs showed corresponding upregulation of adipogenic transcription factors and downregulation of mitochondrial biogenesis genes. Integrated transcriptomic and whole-genome bisulfite sequencing (WGBS) analyses revealed nuclear transcriptional reprogramming that was closely associated with differential DNA methylation, predominantly affecting mitochondrial function and lipid metabolism pathways. Mitopig fibroblasts also showed a pro-inflammatory response to lipopolysaccharide stimulation, with elevated expression of IL-12, NOS2, RELA, and TNF-α. Our findings provide direct in vivo evidence that mtDNA variants regulate adiposity in pigs through mitochondrial dysfunction, oxidative stress, and nuclear epigenetic modulation, highlighting the potential for incorporating mtDNA haplotype information into pig breeding programs as a complementary strategy to nuclear genomic selection. - Source: PubMed
Publication date: 2026/09/05
Liu HaoJiang YunliangShi WenshuYan ChaoOuyang ZhaochaoZhang XinGuo YanshunGuo ZhongjuLi QiuyanZhao Xingbo - is an edible medicinal fungus with potential metabolic benefits, but its effects on type 2 diabetes mellitus accompanied by hyperlipidaemia (T2DM-HLP) remain incompletely understood. This study evaluated the effects of orally administered ethanol extract (EAE; 2.0 g kg) and cordycepin (50 or 100 mg kg) in a T2DM-HLP mouse model over 6 weeks. Metabolic indices, serum transaminases, colon and liver histology, gut bacterial and fungal communities, serum metabolites, and FXR/TGR5-related molecular markers were assessed. Compared with the model group, EAE and 50 mg kg cordycepin reduced serum lipid and transaminase levels to varying degrees and were associated with downward shifts in fasting blood glucose and oral glucose tolerance test curves. Histological alterations in the colon and liver were also less apparent in these two groups. Faecal 16S rDNA and ITS sequencing showed changes in the bacterial and fungal community structure, while untargeted serum metabolomics identified distinct metabolic profiles involving bile acids, fatty acids, amino acids, nucleotides, and redox-related metabolites. Enrichment analyses implicated bile secretion, primary bile acid biosynthesis, cholesterol metabolism, cAMP signalling, and amino acid metabolism. These changes were accompanied by increased colonic TGR5 and hepatic FXR immunoreactivity, increased hepatic , , and expression, and reduced expression. Responses to 100 mg kg cordycepin were less consistent, indicating no simple dose-dependent relationship under the present conditions. Overall, EAE and cordycepin were associated with improved metabolic status and coordinated changes in the gut microbial composition, serum metabolism, and bile acid-related molecular readouts. - Source: PubMed
Publication date: 2026/09/04
Shi HuaijieMeng YingZhang GuoyingLing Jianya - Nonalcoholic steatohepatitis (NASH) is the progressive stage of nonalcoholic fatty liver disease characterized by varying degrees of inflammation, hepatic steatosis, liver cell damage and fibrosis, which can seriously harm people's health. Shenling Baizhu (SL) powder exhibits a strong capacity to modulate cellular mechanisms, thereby demonstrating exceptional potential in addressing inflammatory and oxidative stress-related pathologies. However, the exact mechanism of SL in NASH has not been fully elucidated. We aimed to explore the therapeutic effect and potential mechanism of SL in NASH mice. - Source: PubMed
Publication date: 2026/08/20
Huang SiyuanDeng YuanjunPi DajinZhou FangyuPan JinyueSong QingliangLiu LianghaoLi YuanyouYang QinhePan MaoxingZhang Yupei - The fibroinflammatory liver microenvironment (FILM), characterized by collagen-rich stroma and immunosuppressive inflammation, is prevalent in hepatocellular carcinoma (HCC) and correlates with poor response to programmed cell death protein 1 (PD-1) blockade. Here, we show that FILM suppresses gasdermin E (GSDME)-dependent pyroptosis and promotes immune suppression and anti-PD-1 resistance. Mechanistically, FILM-associated cancer-associated fibroblasts recruit and polarize macrophages toward a nitric oxide synthase 2 (NOS2)⁺ inflammatory phenotype. NOS2+ macrophage-derived nitric oxide induces SP1 S-nitrosylation, impairs SP1 binding to the peroxisome proliferator-activated receptor alpha (PPARA) promoter and transcriptionally represses PPARA in HCC cells. PPARα downregulation reduces pyruvate dehydrogenase kinase 4 (PDK4) expression, mitochondrial reactive oxygen species production, caspase-3 activation and GSDME cleavage. Conversely, ligand activation of tumor intrinsic PPARα restores the PDK4-ROS-caspase-3-GSDME axis, enhances dendritic cell and CD8⁺ T cell activation, and sensitizes HCC to anti-PD-1 therapy. The clinically approved PPARα agonist fenofibrate enhances anti-PD-1 efficacy in HCC models in male mice and is associated with improved clinical benefit in a retrospective cohort of patients with HCC. We propose a FILM-NOS2-SP1-PPARα-PDK4 axis that controls pyroptotic immunogenicity and immunotherapy response, supporting PPARα activation as a strategy to overcome FILM-associated immune resistance in HCC. - Source: PubMed
Publication date: 2026/08/06
Chen PengXiong KaiHuang KuiyuanDong ZheyuLiang JunjieGan XiaoningLi TengzhenZhang MorangJing ShunziXu XinwenZheng YaluLi ZhangyunChen WeicongZheng DandanZhong YuanyuanDai GuanqiLi QiangChu JiaojiaoCao MingrongSun JianLiu ZhilongLi JiexinChen ShangxiangZhao YuanboJuan QinLi XueqinWen ZhiliLi YongyinPang HuajinWang DuoJiang Yuchuan - Ultraviolet B radiation (UVB) in sunlight is classified by the WHO as a Group 1 carcinogen. UVB is readily absorbed by the epidermis, and excessive exposure causes skin injury and photoaging. Peroxisome proliferator-activated receptor α (PPARα), a key member of the nuclear receptor family, plays a central role in lipid metabolism. This study aims to observe and investigate the effects of PPARα deletion on the progression of UVB-induced damage and changes in the skin lipid profile using -knockout ( ) and wild-type mice. - Source: PubMed
Jiang FengdiLiu YifanWang MingyuXie XiaotaoMaheliya AdiliDu MengjieWang JiajiaXiong HaiZhang Shuyu