Ask about this productRelated genes to: FGF21 Blocking Peptide
- Gene:
- FGF21 NIH gene
- Name:
- fibroblast growth factor 21
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1999-11-26
- Date modifiied:
- 2014-11-18
Related products to: FGF21 Blocking Peptide
Related articles to: FGF21 Blocking Peptide
- Mitokines play a critical role in maintaining cognitive function and promoting healthy aging by modulating systemic responses to cellular stress. This study examined the effects of three exercise modalities, including Sprint Interval Training (SIT), High-Intensity Interval Training (HIIT), and Moderate-Intensity Continuous Training (MICT), on mitokine expression and cognitive performance in the D-galactose-induced aging rat model. A total of 35 male Wistar rats were included: 7 as healthy control, and 28 received D-galactose (150 mg/kg/day for 8 weeks) then randomly divided into D-gal, MICT, HIIT, and SIT (n=7 each). Exercise training was performed five days per week for eight weeks. Protocols included HIIT (85% vVO), MICT (60% vVO), and SIT (4-9 × 10 s at 118-165% vVO₂max). FGF21 and GDF15 protein levels were measured by Western blotting. Cognitive function was evaluated using the passive avoidance test, and histological changes were assessed via H&E staining. The results demonstrated that HIIT markedly elevated FGF21 protein expression compared to both the D-gal and other exercise groups (p < 0.0001), suggesting superior mitochondrial and metabolic adaptation. In contrast, the D-galactose group exhibited the highest levels of GDF15, with significant reductions observed in the HIIT and MICT groups relative to SIT. All exercise protocols led to a significant increase in step-through latency (p < 0.0001) and a marked reduction in the time spent in the dark chamber (p < 0.0001), both indicative of improved aversive memory in the passive avoidance task. These findings support the notion that HIIT optimally modulates mitokine activity to promote mitochondrial health and cognitive function. In addition to molecular adaptations, behavioral improvements such as enhanced memory performance further underscore exercise as a viable strategy for mitigating age-related impairments. - Source: PubMed
Publication date: 2026/06/06
Alizade SafouraFaramarzi MohammadThapa Rohit KumarBeheshti Siamak - Transfusion-dependent β-thalassemia (TDT) is characterized by reduced exercise capacity due to chronic hemolytic anemia, iron overload cardiomyopathy, and potential skeletal muscle alterations. Early cardiovascular and muscular dysfunction in the absence of cardiac iron overload remains poorly characterized. - Source: PubMed
Publication date: 2026/06/06
Braggio MicheleCeolan JacopoMinoia AriannaVillaboni SimoneMazzi FilippoFederti EnricaValenti Maria TeresaFranceschi Lucia DeCarbonare Luca DalleCominacini Mattia - Obesity is associated with metabolic dysfunction-associated steatotic liver disease (MASLD), for which drugs and nutraceuticals are being developed. We investigated whether camelina seeds from the Brassicaceae family and their components can attenuate metabolic disorders in animal models of genetic obesity, including fatty liver. - Source: PubMed
Publication date: 2026/06/06
Jurgoński AdamOpyd Paulina MNapiórkowska DorotaFotschki BartoszBrzuzan Łucja - Previous studies have indicated that Valsartan (Val) modulates peroxisome proliferator-activated receptor α (PPARα) expression in the liver; however, its precise roles in liver injury, both pathological and physiological, remain unclear, necessitating further investigation. This study hypothesises that FGF21 mediates Val's hepatoprotective effects in acetaminophen (APAP)-induced acute liver injury. The results demonstrate that fibroblast growth factor 21 (FGF21) is a key mediator of Val-induced hepatoprotection, acting through the activation of the peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α)/ nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant pathway. This finding reveals a previously unrecognised physiological role for Val beyond its established antihypertensive effects. In a murine model of acute liver injury, Val treatment significantly alleviated APAP-induced hepatic necrosis and oxidative stress, leading to improved survival outcomes. However, the hepatoprotective effects of Val were markedly reduced in FGF21 knockdown models and partially restored following FGF21 reconstitution. Notably, Val maintained considerable efficacy after angiotensinIItype1receptor (AT1R) silencing. In contrast, pharmacological inhibition of the PPARα pathway significantly suppressed Val-induced FGF21 activation and its downstream signalling events. Mechanistically, Val increases hepatic FGF21 expression, which activates the PGC-1α/Nrf2 pathway to counter oxidative damage. In conclusion, these findings position FGF21 as a key mediator of Val-induced hepatoprotection, supporting its repositioning for acute liver injury and expanding Val's clinical applications beyond hypertension to liver-related conditions. - Source: PubMed
Publication date: 2026/06/04
Zheng JunweiHan BingyanWang SuntaoDong LingjiaJin JiajiaWang KaichengHai DarongYang MinaXu YanyanPan JingyePan Xuebo - Metabolic dysfunction-Associated Steatohepatitis (MASH) is a progressive subtype of Metabolic dysfunction-Associated Steatotic Liver Disease (MASLD) characterized by hepatic steatosis, inflammation, hepatocellular injury, and fibrosis, which may evolve to cirrhosis and hepatocellular carcinoma. Despite its growing global burden, no widely approved pharmacotherapy is available, highlighting the need to elucidate immunometabolic mechanisms and identify effective therapeutic targets. - Source: PubMed
Publication date: 2026/05/20
Yu JiangPeng Yong