FGF21 (Fibroblast Growth Factor 21)

HO-1 showed a significant inverse correlation with HMGB-1 (r = -0.405, p = 0.001), KEAP1 was positively correlated with sST2 (r = 0.282, p = 0.029), and GPX4 was correlated with FGF21 (r = 0.255, p = 0.049); no other significant associations were found. β-thalassemia major patients exhibit significant endothelial and cardiac injury markers, altered lipid profiles, and selective upregulation of antioxidant and ferroptosis-related genes.

In this group of patients with MASLD, sASGR1 levels are higher and are associated with the occurrence of MASLD, suggesting that sASGR1 may be an independent risk factor for MASLD.

Conversely, GDF15 and IL-6 exhibit context-dependent variability. Further prospective cohort studies are warranted to better understand these adipokines, as persons with normal weight may still be at a high risk of cardiometabolic diseases.

The aim of this narrative review was to elucidate the complex interplay between myokines, adipokines, inflammation, and insulin resistance, and to clarify their clinical relevance in metabolic and thyroid disorders. Given this integrative role of SM, sarcopenia should be recognized as a clinical marker of metabolic or thyroid dysregulation, and preserving muscle mass through structured physical activity should be a core therapeutic target.

Notably, myokine secretion varies with muscle fiber type, influencing their specific biological effects. Understanding how myokines are regulated and function may support the development of new therapies in regenerative medicine, oncology, and metabolic disease treatment.

Collectively, these molecular adaptations establish exercise as a systemic biological stimulus capable of restoring metabolic homeostasis and counteracting the pathophysiological processes underlying NCDs. Understanding these mechanisms provides a foundation for developing targeted, personalized exercise-based interventions in preventive and therapeutic medicine.

After IL-17A addition to PDAC cell lines, the inhibitory effect of FGF21 on the Notch signaling pathway was significantly reduced. FGF21 suppresses invasion and metastasis in PDAC by inhibiting the IL-17A-Notch signaling axis, which reveals a novel therapeutic strategy for this malignancy.

Among β-thalassemia major patients (7-35 years), 73.3% (n = 44/60) were splenectomized; 36 received deferiprone, 19 deferasirox, and 5 deferoxamine. Endocrine disturbances are common in β-thalassemia major despite chelation therapy. Incorporating endocrine assessment into routine practice is essential for early detection and management.

Because elevated FGF21 during liver stress may indicate significant metabolic disruption, our data provides strong evidence that FGF21 may represent a valuable prognostic and potentially therapeutic biomarker in HCC. Future independent studies are required to validate our results.

Several pharmacological agents including incretin-based strategies, FGF21 analogues and the panPPAR agonist lanifibranor target the interface of MASLD and T2DM and have thereby shown promise to improve MASH and associated liver fibrosis. In light of the evident close multilevel links between MASLD and T2DM, care development efforts for MASLD in guidelines, local protocols and implementation strategies should aim to involve hepatologists, diabetologists, PCPs and their affiliated care teams in a joint effort to address the growing burden of fibrotic MASLD.

Wnt/β-catenin signaling could be a potential lymphomagenetic mechanism for extranodal infiltration of T-lymphoblastic lymphoma. Fenofibrate has the potential to be an effective therapeutic strategy against liver infiltration of T-lymphoblastic lymphoma in MASH liver.