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
- Hepatic diseases pose a major and life-threatening global health challenge. Sesaminol, a sesame-seed lignan with antioxidant and anti-inflammatory properties, was investigated for its ability to combat metabolic dysfunction-associated fatty liver disease (MAFLD) and alcohol-related liver injury. Mice fed a high-fat diet (HFD) or subjected to binge alcohol injury received oral sesaminol to evaluate its protective effects against hepatic dysfunction. Complementary in vitro studies used HepG2 cells to delineate the potential mechanism. Sesaminol reduced body-weight gain, enhanced glucose tolerance and insulin signaling, lowered hepatic and serum lipid accumulation, and attenuated the inflammatory response in mice. Moreover, sesaminol dose-dependently reduced triglyceride (TG) accumulation and suppressed pro-inflammatory cytokines in vitro. Transcriptomic and docking analyses identified peroxisome proliferator-activated receptor alpha (PPARα) as a direct sesaminol target and revealed solute carrier family 27 member 5 (Slc27a5) as a novel downstream gene. Sesaminol enhanced PPARα occupancy on the Slc27a5 promoter, increased fatty acid uptake, and restored mitochondrial β-oxidation flux. Therefore, sesaminol may function as a natural PPARα agonist that links fatty acid import to mitochondrial oxidation via Slc27a5, thereby ameliorating hepatic steatosis and inflammation in both metabolic and alcohol-related liver dysfunction. - Source: PubMed
Zheng LiujieZhou JunJin HaojieLong YuZheng YifanDing KunyingZheng ZiyiZhuge FenFu ZhengweiNi Yinhua - Type 2 diabetes (T2D) is a multifactorial disease characterized by insulin resistance and chronic low-grade inflammation. Although treatments are available, they are often ineffective and cause side effects in patients. Ginger (Zingiber officinale) has demonstrated antidiabetic potential; however, the molecular mechanisms underlying its bioactive compounds remain incompletely understood. - Source: PubMed
Publication date: 2026/05/17
Martínez-Esquivias FernandoPech-Santiago Edar OGuzmán-Flores Juan ManuelAnaya-Esparza Luis MiguelMendez-Robles Maria DoloresChávez-Díaz Ismael Fernando - A recent study reported that endothelial PAS domain protein 1 (EPAS1; hypoxia-inducible factor 2α) acts downstream of PGC-1α to regulate the slow-twitch muscle fiber program in mice, yet its role in human physiology and exercise adaptation remains unclear. The aim of this study was threefold: (1) to investigate EPAS1 gene expression in human skeletal muscle and its association with muscle fiber composition and the expression of endurance-related genes; (2) to determine how EPAS1 expression responds to aerobic training; and (3) to examine whether EPAS1 genetic variation is linked to aerobic capacity, hemoglobin, and athletic status. The study involved 1234 subjects, including 943 athletes and 291 untrained individuals. EPAS1 gene expression was significantly higher in endurance athletes compared with power athletes (p = 0.011) and was positively associated with the proportion of slow-twitch muscle fibers in the vastus lateralis of untrained subjects (p = 0.0008) and athletes (p = 0.0033). EPAS1 expression was higher in females (p = 0.0028) and negatively associated with smoking status (p = 0.0007). Moreover, EPAS1 expression showed positive association with endurance-related genes, including ANGPT2, CKM, CPT1B, EPOR, FNDC5, HIF1A, KDR, MYBPC3, NFATC4, NOS3, PPARA, PPARD, PPARGC1A, UCP2, and VEGFA. Analysis of 24 publicly available skeletal muscle transcriptomic datasets demonstrated that EPAS1 expression increased significantly (meta-analysis p = 9.2 × 10) following aerobic training. Finally, genetically predicted higher EPAS1 expression (i.e., carriage of the EPAS1 rs6756667 A allele) was positively associated with endurance athlete status in both sexes (p = 0.0004) and with VO₂max (p = 0.046) and hemoglobin (p = 0.041) in male athletes. These findings potentially identify EPAS1 as an important genetic factor associated with muscle fiber composition, endurance-related phenotypes, and adaptation to aerobic training. - Source: PubMed
Dautova Albina ZValeeva Elena VSemenova Ekaterina AMavliev Fanis AZverev Alexey ANazarenko Andrey SJohn GeorgeZhelankin Andrey VLarin Andrey KKulemin Nikolay ASultanov Rinat IGenerozov Edward VAhmetov Ildus I - Limb ischemia-reperfusion (I/R) injury is a life-threatening complication of acute limb ischemia that can result in severe skeletal muscle damage and limb loss, yet effective pharmacological therapies remain limited. Kaempferol (KAE), a naturally occurring dietary flavonoid with well-documented anti-inflammatory, antioxidant, and anti-apoptotic properties, has been shown to confer protection in myocardial and cerebral I/R models. Nevertheless, its therapeutic potential and molecular mechanisms in limb I/R injury have not yet been elucidated. In this study, we systematically investigated the protective effects and underlying mechanisms of KAE in a mouse hindlimb I/R model. A network pharmacology approach was initially applied to provide a global overview of potential biological processes associated with KAE treatment. The therapeutic efficacy and molecular mechanisms of KAE were subsequently evaluated using in vivo experiments combined with transcriptomic profiling. Mice subjected to 4 h of hindlimb ischemia followed by 24 h of reperfusion received KAE (50 or 100 mg/kg, intraperitoneally) for 7 consecutive days prior to I/R induction. KAE markedly improved hindlimb microcirculation, alleviated tissue edema and infarction, preserved muscle histological integrity, and attenuated elevations of circulating muscle injury biomarkers. In parallel, KAE significantly suppressed I/R-induced oxidative stress, inflammatory infiltration, and apoptotic cell death, as evidenced by reduced ROS accumulation, decreased pro-inflammatory cytokine expression, and favorable modulation of apoptosis-related proteins. Transcriptomic analysis revealed pronounced activation of inflammatory pathways and suppression of the PPAR signaling pathway following limb I/R injury, whereas KAE treatment selectively restored PPAR pathway activity while inhibiting NF-κB signaling. qRT-PCR and Western blot analyses further demonstrated that KAE predominantly upregulated PPARα expression and reduced NF-κB p65 phosphorylation in reperfused skeletal muscle. Collectively, these findings provide comprehensive evidence that KAE protects against hindlimb I/R injury, with activation of PPARα signaling and concomitant suppression of NF-κB-driven inflammation representing a proposed mechanism, thereby supporting KAE as a promising pharmacological candidate for limb I/R injury. - Source: PubMed
Liu YueheLin MuliangQian HongWang WeiweiYuan TaoRen ZhengrongHu JianlunWang YangLiu GuoyinSun ZhongyangGou PengSun ZhaoruiChen YuanyuanSun YanHe YunfeiYu XinNie Shinan - - Source: PubMed
Publication date: 2026/05/14
Zhang ZhengTang En-QiLi Chun-HuiWang Bi-BiLiang YueLv Jin-XinChen Gao-FengLiu WeiMu Yong-PingLiu PingChen Jia-Mei