Evidence map›Paper›PMID 40664344›Full record

ReviewPharmacological research2025

Fibroblast growth factor 16: Molecular mechanisms, signalling crosstalk, and emerging roles in cardiac biology and metabolic regulation.

Xiaodan Hui, Qian Lin, Kaiqing Liu, Chunjie Gu, Ahmed Abdelbaset-Ismail, Kupper A Wintergerst, Zhongbin Deng, Lu Cai, Yi Tan

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Pharmacological research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Xiaodan HuiPediatric Research Institute, Departments of Pediatrics, University of Louisville School of Medicine, Louisville, KY, USA.
Qian LinTouchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Kaiqing LiuPediatric Research Institute, Departments of Pediatrics, University of Louisville School of Medicine, Louisville, KY, USA.
Chunjie GuPediatric Research Institute, Departments of Pediatrics, University of Louisville School of Medicine, Louisville, KY, USA.
Ahmed Abdelbaset-IsmailPediatric Research Institute, Departments of Pediatrics, University of Louisville School of Medicine, Louisville, KY, USA.
Kupper A WintergerstWendy Novak Diabetes Institute, Norton Children's Hospital, Louisville, KY, USA; Norton Children's Endocrinology, Department of Pediatrics, University of Louisville, Norton Children's Hospital, Louisville, KY, USA; The Center for Integrative Environmental Health Sciences, University of Louisville School of Medicine, Louisville, KY, USA.
Zhongbin DengDepartment of Surgery, Division of Immunotherapy, University of Louisville School of Medicine, KY, USA; Brown Cancer Center, University of Louisville School of Medicine, Louisville, KY, USA.
Lu CaiPediatric Research Institute, Departments of Pediatrics, University of Louisville School of Medicine, Louisville, KY, USA; Wendy Novak Diabetes Institute, Norton Children's Hospital, Louisville, KY, USA; The Center for Integrative Environmental Health Sciences, University of Louisville School of Medicine, Louisville, KY, USA; Department of Pharmacology and Toxicology, University of Louisville School of Medicine, Louisville, KY 40202, USA; Department of Radiation Oncology, University of Louisville School of Medicine, Louisville, KY, USA.
Yi TanPediatric Research Institute, Departments of Pediatrics, University of Louisville School of Medicine, Louisville, KY, USA; Wendy Novak Diabetes Institute, Norton Children's Hospital, Louisville, KY, USA; Department of Pharmacology and Toxicology, University of Louisville School of Medicine, Louisville, KY 40202, USA. Electronic address: yi.tan@louisville.edu.

Funding

University of Louisville Center for Integrative Environmental Health SciencesP30ES030283 · NIEHS · UNIVERSITY OF LOUISVILLE · PI Amanda Jo LeBlanc · 2020 to 2026
$10.0M
Fibroblast Growth Factor 1 Prevents Hyperlipidemia and atherosclerosisR01HL160927 · NHLBI · UNIVERSITY OF LOUISVILLE · PI Yi Tan · 2022 to 2026
$2.7M
Dual targeting chemokine receptors prevents chemotherapy-induced cardiotoxicityR01HL174922 · NHLBI · UNIVERSITY OF LOUISVILLE · PI Yi Tan · 2024 to 2026
$2.0M
CSN8 regulation of S1P-enriched extracellular vesicles to modulate NAFLD by gut-liver axisR01DK115406 · NIDDK · UNIVERSITY OF LOUISVILLE · PI DENG, ZHONG-BIN · 2018 to 2022
$2.0M
A novel mechanism of stromal cell-derived factor 1 protection against diabetic cardiomyopathyR01HL125877 · NHLBI · UNIVERSITY OF LOUISVILLE · PI TAN, YI · 2017 to 2021
$1.9M
The role of neutral ceramidase in intestinal fucosylation and liver steatosis and inflammationR01DK131442 · NIDDK · UNIVERSITY OF LOUISVILLE · PI Zhong-Bin Deng · 2022 to 2026
$1.6M
NHLBI NIH HHS R01 HL125877NHLBI NIH HHS R01 HL160927NHLBI NIH HHS R01 HL174922NIDDK NIH HHS R01 DK115406NIDDK NIH HHS R01 DK131442NIEHS NIH HHS P30 ES030283
6 · The paper itself

Abstract

Fibroblast growth factor (FGF) 16 is critically involved in embryonic heart development, adult cardiac homeostasis, and potentially in metabolic regulation. Initially recognized for its cardiac-specific role during embryogenesis, recent studies demonstrate that FGF16 significantly mitigates pathological cardiac remodelling, such as fibrosis and hypertrophy, through competitive inhibition of FGF2-induced transforming growth factor-β1 signalling via FGF receptor 1c. Molecular investigations further indicate that FGF16 exerts cardioprotective effects primarily through activation of key intracellular pathways, including phosphoinositide 3-kinase/protein kinase B and protein kinase C, as well as regulation by transcription factors GATA binding protein 4, nuclear Factor kappa-light-chain-enhancer of activated B cells, and cardiac-specific homeobox/NK2 homeobox 5, and RNA methyltransferase-mediated N6-methyladenosine modifications. However, detailed mechanisms underlying receptor-specific interactions remain unclear. This review systematically summarizes the genomic organization, receptor selectivity, cardiac signalling mechanisms, and emerging metabolic roles of FGF16, critically evaluates the current evidence, identifies key research gaps, and highlights therapeutic potentials for cardiovascular and metabolic disorders.

Indexed as

Fibroblast Growth FactorsHeartMyocardiumAnimalsHumansSignal TransductionFibroblast Growth FactorsCardiac DevelopmentCardiac RemodellingFGF16Metabolic RegulationSignalling Crosstalk

Identifiers

PMID40664344
PMCPMC12392149

What OpenQuestion holds

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Registered trials

None linked

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.