Exercise-Induced Fibroblast Growth Factor-21: A Systematic Review and Meta-Analysis

Kim, Hyunjoong; Jung, Jihye; Park, Sungeon; Joo, Younglan; Lee, Sangbong; Shim, Jung Woo; Choi, Jinhyeong; Lee, Hyun; Hwang, Gyujeong; Lee, Seungwon

doi:10.3390/ijms24087284

Cited by 7 publications

(5 citation statements)

References 68 publications

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“…The FGF and FGFR (fibroblast growth factor receptor) signaling systems regulate exercise-induced cardiac hypertrophy. 59 However, current research has primarily focused on FGF2 60 and FGF21, 61 neglecting FGF5. Furthermore, large prospective studies are needed to investigate the role of FGF5.…”

Section: Discussionmentioning

confidence: 99%

Identification of Circulating Plasma Proteins as a Mediator of Hypertension-Driven Cardiac Remodeling: A Mediation Mendelian Randomization Study

Hu,

Lin,

Zhang

et al. 2024

Hypertension

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BACKGROUND: This study focused on circulating plasma protein profiles to identify mediators of hypertension-driven myocardial remodeling and heart failure. METHODS: A Mendelian randomization design was used to investigate the causal impact of systolic blood pressure (SBP), diastolic blood pressure (DBP), and pulse pressure on 82 cardiac magnetic resonance traits and heart failure risk. Mediation analyses were also conducted to identify potential plasma proteins mediating these effects. RESULTS: Genetically proxied higher SBP, DBP, and pulse pressure were causally associated with increased left ventricular myocardial mass and alterations in global myocardial wall thickness at end diastole. Elevated SBP and DBP were linked to increased regional myocardial radial strain of the left ventricle (basal anterior, mid, and apical walls), while higher SBP was associated with reduced circumferential strain in specific left ventricular segments (apical, mid-anteroseptal, mid-inferoseptal, and mid-inferolateral walls). Specific plasma proteins mediated the impact of blood pressure on cardiac remodeling, with FGF5 (fibroblast growth factor 5) contributing 2.96% ( P =0.024) and 4.15% ( P =0.046) to the total effect of SBP and DBP on myocardial wall thickness at end diastole in the apical anterior segment and leptin explaining 15.21% ( P =0.042) and 23.24% ( P =0.022) of the total effect of SBP and DBP on radial strain in the mid-anteroseptal segment. Additionally, FGF5 was the only mediator, explaining 4.19% ( P =0.013) and 4.54% ( P =0.032) of the total effect of SBP and DBP on heart failure susceptibility. CONCLUSIONS: This mediation Mendelian randomization study provides evidence supporting specific circulating plasma proteins as mediators of hypertension-driven cardiac remodeling and heart failure.

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Section: Discussionmentioning

confidence: 99%

Identification of Circulating Plasma Proteins as a Mediator of Hypertension-Driven Cardiac Remodeling: A Mediation Mendelian Randomization Study

Hu,

Lin,

Zhang

et al. 2024

Hypertension

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“…Through PPARg-mediated transcriptional activation, exercise induces adipose expression of FGFR1 and bklotho, sensitizing FGF21 actions in adipose tissues to send humoral signals for multi-organ crosstalk, thereby maintaining metabolic homeostasis (80). A systematic review, involving 376 participants from 10 studies, demonstrated a significant increase in FGF-21 levels after exercise compared to no exercise (81). Longterm aerobic exercise has been observed to lower human FGF21 levels and is associated with an improvement in FGF21 resistance (34).…”

Section: Fgf21 Is a Potential Target For Dkd Therapymentioning

confidence: 99%

Critical role of FGF21 in diabetic kidney disease: from energy metabolism to innate immunity

Liang,

Chen,

Chang

et al. 2024

Front. Immunol.

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Diabetic kidney disease (DKD) stands as the predominant cause of chronic kidney disease (CKD) on a global scale, with its incidence witnessing a consistent annual rise, thereby imposing a substantial burden on public health. The pathogenesis of DKD is primarily rooted in metabolic disorders and inflammation. Recent years have seen a surge in studies highlighting the regulatory impact of energy metabolism on innate immunity, forging a significant area of research interest. Within this context, fibroblast growth factor 21 (FGF21), recognized as an energy metabolism regulator, assumes a pivotal role. Beyond its role in maintaining glucose and lipid metabolism homeostasis, FGF21 exerts regulatory influence on innate immunity, concurrently inhibiting inflammation and fibrosis. Serving as a nexus between energy metabolism and innate immunity, FGF21 has evolved into a therapeutic target for diabetes, nonalcoholic steatohepatitis, and cardiovascular diseases. While the relationship between FGF21 and DKD has garnered increased attention in recent studies, a comprehensive exploration of this association has yet to be systematically addressed. This paper seeks to fill this gap by summarizing the mechanisms through which FGF21 operates in DKD, encompassing facets of energy metabolism and innate immunity. Additionally, we aim to assess the diagnostic and prognostic value of FGF21 in DKD and explore its potential role as a treatment modality for the condition.

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“…Promotes Fiber-Type Remodeling, Inhibits TGF-β1-Smad2/3-mmp9, and Activates p38 MAPK Signaling Pathway in C2C12 Myotubes Fgf21, primarily secreted by the liver and also produced in other tissues including muscle, is known to enhance the function of mitochondria, the cellular components responsible for energy production, potentially impacting muscle fiber type indirectly [25,26]. To investigate the direct role of Fgf21 in regulating muscle fiber types, we performed immunoblot analysis of MyHC I, MyHC IIa, MyHC IIb, TGF-β1, Smad2/3, mmp2, mmp9, and p-p38 proteins in C2C12 cells.…”

Section: Fgf21mentioning

confidence: 99%

Endurance Exercise-Induced Fgf21 Promotes Skeletal Muscle Fiber Conversion through TGF-β1 and p38 MAPK Signaling Pathway

Luo

Zhang

Cao

et al. 2023

IJMS

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Fgf21 has been identified as playing a regulatory role in muscle growth and function. Although the mechanisms through which endurance training regulates skeletal muscle have been widely studied, the contribution of Fgf21 remains poorly understood. Here, muscle size and function were measured, and markers of fiber type were evaluated using immunohistochemistry, immunoblots, or qPCR in endurance-exercise-trained wild-type and Fgf21 KO mice. We also investigated Fgf21-induced fiber conversion in C2C12 cells, which were incubated with lentivirus and/or pathway inhibitors. We found that endurance exercise training enhanced the Fgf21 levels of liver and GAS muscle and exercise capacity and decreased the distribution of skeletal muscle fiber size, and fast-twitch fibers were observed converting to slow-twitch fibers in the GAS muscle of mice. Fgf21 promoted the markers of fiber-type transition and eMyHC-positive myotubes by inhibiting the TGF-β1 signaling axis and activating the p38 MAPK signaling pathway without apparent crosstalk. Our findings suggest that the transformation and function of skeletal muscle fiber types in response to endurance training could be mediated by Fgf21 and its downstream signaling pathways. Our results illuminate the mechanisms of Fgf21 in endurance-exercise-induced fiber-type conversion and suggest a potential use of Fgf21 in improving muscle health and combating fatigue.

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Exercise-Induced Fibroblast Growth Factor-21: A Systematic Review and Meta-Analysis

Cited by 7 publications

References 68 publications

Identification of Circulating Plasma Proteins as a Mediator of Hypertension-Driven Cardiac Remodeling: A Mediation Mendelian Randomization Study

Identification of Circulating Plasma Proteins as a Mediator of Hypertension-Driven Cardiac Remodeling: A Mediation Mendelian Randomization Study

Critical role of FGF21 in diabetic kidney disease: from energy metabolism to innate immunity

Endurance Exercise-Induced Fgf21 Promotes Skeletal Muscle Fiber Conversion through TGF-β1 and p38 MAPK Signaling Pathway

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