FGF21 protein
- Known as:
- FGF21 protein
- Catalog number:
- 80R-4397
- Product Quantity:
- 50 ug
- Category:
- -
- Supplier:
- Fitzgerald
- Gene target:
- FGF21 protein
Related genes to: FGF21 protein
- 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 protein
Related articles to: FGF21 protein
- Cardiovascular-kidney-metabolic (CKM) syndrome is a multisystem disorder in which obesity, diabetes, chronic kidney disease, and cardiovascular disease reinforce one another through shared pathobiological characteristics and bidirectional organ crosstalk. Rather than representing the mere coexistence of diseases, CKM syndrome can be understood as a mitochondrial systems disorder. In energy-intensive tissues such as the myocardium and renal tubules, chronic haemodynamic stress, substrate excess, hypoxia and neurohormonal activation converge on mitochondrial programmes governing oxidative phosphorylation, redox balance, organelle dynamics and quality control. Disruption of these programmes, including impaired fatty acid oxidation, suppressed biogenesis, defective mitophagy and mitochondrial DNA instability, reduces bioenergetic reserve and promotes reactive oxygen species generation, inflammatory signalling and progressive organ dysfunction. Mitochondrial dysfunction in other metabolic tissues further amplifies these processes. In the liver, reduced fatty acid oxidation promotes steatosis, insulin resistance and the release of lipids, whereas in skeletal muscle and adipose tissue, impaired oxidative capacity and insulin resistance increases lipid spillover and systemic inflammation. Mitochondria-derived signals - including FGF21, GDF15, succinate and circulating mitochondrial DNA - enable bidirectional communication between organs, reinforcing multi-organ decline in a positive-feedback loop. Advancing our understanding of mitochondrial dysfunction and inter-organ communication may provide new mechanistic insights into CKM syndrome progression and inform the development of mitochondria-targeted therapeutic strategies. - Source: PubMed
Publication date: 2026/09/24
Li ShenAbel E DaleArany ZoltanBaur Joseph APei LimingSusztak Katalin - To investigate the relationships among the expression levels of serum silencing information regulator 2-related enzyme 1 (SIRT1), endothelial cell-specific molecule-1 (ESM-1), and fibroblast growth factor-21 (FGF21) and treatment results in patients with acute respiratory distress syndrome (ARDS) associated with sepsis. - Source: PubMed
Peng CanSun ZhigangLiu YanyanLiu YouguiZhao Hao - Type 2 diabetes (T2D) is a major global health challenge, primarily driven by insulin resistance and progressive β-cell dysfunction aggravated by chronic low-grade inflammation. Skeletal muscle has emerged as a pivotal endocrine organ through the secretion of myokines, which exert systemic metabolic and immunomodulatory effects. - Source: PubMed
Publication date: 2026/09/22
Tague ChristianMakeda DujardinYokolo HermannEkouo Joshua - Metabolic dysfunction-associated steatotic liver disease (MASLD) is a progressive liver disorder characterized by inflammation, fibrosis, and metabolic dysfunction. In recent years, therapeutic options have expanded significantly. The thyroid hormone receptor-β agonist resmetirom became the first drug approved in Germany in 2025 for non-cirrhotic MASH with moderate to advanced fibrosis. Furthermore, incretin mimetics, originally developed for diabetes and obesity, are being investigated. In a phase 3 study, semaglutide demonstrated significant improvements in hepatic inflammation and fibrosis. Beyond GLP-1 analogs, which act indirectly through metabolic pathways, several liver fibrosis-specific therapies are emerging, including FGF-21 analogs and dual incretin receptor agonists (e.g. survodutide) that directly affect hepatocytes via glucagon receptor signaling. Combination therapies are increasingly being explored to harness synergistic effects and enable individualized treatment. Ongoing phase 3 studies assess long-term efficacy and safety. In parallel, biomarkers are being refined for patient selection and treatment monitoring. The German SLD Registry will collect patient data and clinical outcomes following the implementation of new therapies. This review summarizes recent advances and future perspectives in the pharmacological treatment of MASH. The combination of metabolic and liver-targeted therapies offers substantial promise for personalized medicine. - Source: PubMed
Publication date: 2026/09/23
Barton AlexanderSchattenberg Jörn M - Metabolic dysfunction-associated steatotic liver disease (MASLD) has become a major global health challenge, largely driven by the increasing prevalence of obesity and type 2 diabetes mellitus. The disease spectrum ranges from isolated steatosis to metabolic dysfunction-associated steatohepatitis (MASH) with progressive fibrosis. Advanced fibrosis substantially increases the risk of cirrhosis, hepatocellular carcinoma, and cardiovascular complications, thereby contributing significantly to morbidity and mortality.Although lifestyle modification remains the cornerstone of therapy, pharmacological treatment is gaining importance in patients with progressive disease or high-risk profiles. Advances in the understanding of MASLD pathophysiology have enabled the development of targeted therapies addressing hepatic lipid accumulation, insulin resistance, inflammation, and fibrogenesis. Promising clinical data have been reported for resmetirom, semaglutide, tirzepatide, survodutide, lanifibranor, and fibroblast growth factor-21 analogues including efruxifermin, pegozafermin, and efimosfermin.This review summarises current and emerging diagnostic and therapeutic strategies and provides practical guidance for clinical management. In addition, a structured treatment algorithm for non-cirrhotic MASLD (F0-F3), restricted to therapies currently available in Europe and stratified according to diabetes status and fibrosis stage, is proposed as an evidence-based tool for routine clinical practice. - Source: PubMed
Publication date: 2026/09/23
Roeb ElkeGeier Andreas