ReviewMolecular biomedicine2026
Biological functions and emerging interplay of FGF21 and GDF15 in metabolic diseases and aging.
Review in Molecular biomedicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Metabolic diseases and age-related disorders represent a major global health burden driven by the increasing prevalence of obesity and obesity-associated complications. These disorders are characterized by chronic disturbances in energy homeostasis. A key feature linking metabolic disease and aging is the activation of stress-related pathways, which contribute to progressive metabolic dysfunction. Among the endocrine mediators of cellular stress, fibroblast growth factor 21 (FGF21) and growth differentiation factor 15 (GDF15) have emerged as key regulators of metabolic homeostasis. Both are induced by similar stress conditions, including nutrient imbalance, inflammation, oxidative and endoplasmic reticulum (ER) stress and mitochondrial dysfunction, and are elevated in pathophysiological conditions such as obesity, type 2 diabetes (T2D), metabolic dysfunction-associated steatotic liver disease (MASLD) and aging. FGF21 and GDF15 also share overlapping regulatory pathways and complementary functions, suggesting a potential coordinated regulation and functional interplay. However, the extent and physiological relevance of this possible interrelationship remain incompletely understood. This review summarizes current knowledge on the regulation, tissue sources, and signaling mechanisms of FGF21 and GDF15 across metabolic diseases and aging, with particular attention to their roles as mediators of adaptive metabolic responses and their overlapping biological actions. We further discuss their context-dependent effects under acute and chronic stress and their relevance as biomarkers of metabolic dysfunction and disease progression. Collectively, this work highlights FGF21 and GDF15 as integrated stress signals linking cellular stress to systemic metabolic adaptation, providing a conceptual framework for understanding their cooperative roles and regulation in metabolic and age-related diseases, which may have therapeutic potential.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.