ArticleCell communication and signaling : CCS2023
FGF19 increases mitochondrial biogenesis and fusion in chondrocytes via the AMPKα-p38/MAPK pathway.
Article in Cell communication and signaling : CCS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.
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
21 citing papers in PubMed, 34 citations in OpenAlex.
- Olink proteomics identifies FGF-19 as a treatment-responsive inflammatory biomarker associated with acupuncture intervention in young females with mild depression.Frontiers in psychiatry · 2026Trial
- Chondrocytes in fracture healing: A review of chondrocyte journey.Chinese medical journal · 2026Review
- FGF19 promotes cartilage destruction in the progress of temporomandibular joint osteoarthritis.Cell and tissue research · 2026Article
- The SDF-1α/CXCR4 axis regulates chondrocyte mitochondrial dynamics via the ERK/AMPKα pathway.Cell communication and signaling : CCS · 2026Article
- Dual-targeted hybrid nanovesicles coordinated bone-muscle regeneration via regulating the DUSP4/p38 MAPK pathway to reverse osteosarcopenia.Journal of nanobiotechnology · 2026Article
- Osteoarthritis: molecular pathogenesis and potential therapeutic options.Signal transduction and targeted therapy · 2026Review
- Microenvironmental stiffness directs microtubule perturbation in chondrocyte mitosis via ILK-refilinB/Smad3 axis.Bone research · 2026Article
- FGF19 in Solid Tumors: Molecular Mechanisms, Metabolic Reprogramming, and Emerging Therapeutic Opportunities.Theranostics · 2026Review
- FGF21 confers neuroprotection in Parkinson's disease by activating the FGFR1-sirt1 pathway.Cellular & molecular biology letters · 2025Article
- The impact of mitochondrial dysfunction on osteoarthritis cartilage: current insights and emerging mitochondria-targeted therapies.Bone research · 2025Review
- A Molecular Chemical Perspective: Mitochondrial Dynamics Is Not a Bystander of Cartilage Diseases.ACS pharmacology & translational science · 2025Review
- The Potential of Mitochondrial Therapeutics in the Treatment of Oxidative Stress and Inflammation in Aging.Molecular neurobiology · 2025Review
- Adult human heart extracellular matrix improves human iPSC-CM function via mitochondrial and metabolic maturation.Stem cells (Dayton, Ohio) · 2025Article
- Association Between Circulating Inflammatory Cytokines and Dentofacial Anomalies.International dental journal · 2025Article
- Fibroblast Growth Factor 19 Disrupts Cartilage Development Via the FGFR4/β-catenin Axis.International journal of biological sciences · 2025Article
- Latest Advances in Chondrocyte-Based Cartilage Repair.Biomedicines · 2024Review
- TGF-β3 mediates mitochondrial dynamics through the p-Smad3/AMPK pathway.Cell proliferation · 2024Article
- Correction: FGF19 increases mitochondrial biogenesis and fusion in chondrocytes via the AMPKα-p38/MAPK pathway.Cell communication and signaling : CCS · 2023Article
- FGF19 induces the cell cycle arrest at G2-phase in chondrocytes.Cell death discovery · 2023Article
- Stiffened fibre-like microenvironment based on patterned equidistant micropillars directs chondrocyte hypertrophy.Materials today. Bio · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibroblast growth factor 19 (FGF19) is recognized to play an essential role in cartilage development and physiology, and has emerged as a potential therapeutic target for skeletal metabolic diseases. However, FGF19-mediated cellular behavior in chondrocytes remains a big challenge. In the current study, we aimed to investigate the role of FGF19 on chondrocytes by characterizing mitochondrial biogenesis and fission-fusion dynamic equilibrium and exploring the underlying mechanism. We first found that FGF19 enhanced mitochondrial biogenesis in chondrocytes with the help of β Klotho (KLB), a vital accessory protein for assisting the binding of FGF19 to its receptor, and the enhanced biogenesis accompanied with a fusion of mitochondria, reflecting in the elongation of individual mitochondria and the up-regulation of mitochondrial fusion proteins. We then revealed that FGF19-mediated mitochondrial biogenesis and fusion required the binding of FGF19 to the membrane receptor, FGFR4, and the activation of AMP-activated protein kinase alpha (AMPKα)/peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1α)/sirtuin 1 (SIRT1) axis. Finally, we demonstrated that FGF19-mediated mitochondrial biogenesis and fusion was mainly dependent on the activation of p-p38 signaling. Inhibition of p38 signaling largely reduced the high expression of AMPKα/PGC-1α/SIRT1 axis, decreased the up-regulation of mitochondrial fusion proteins and impaired the enhancement of mitochondrial network morphology in chondrocytes induced by FGF19. Taking together, our results indicate that FGF19 could increase mitochondrial biogenesis and fusion via AMPKα-p38/MAPK signaling, which enlarge the understanding of FGF19 on chondrocyte metabolism. Video Abstract.
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.