Evidence map›Paper›PMID 35351862›Full record

ArticleCell death & disease2022

Fibroblast growth factor 20 attenuates pathological cardiac hypertrophy by activating the SIRT1 signaling pathway.

Yunjie Chen, Ning An, Xuan Zhou, Lin Mei, Yanru Sui, Gen Chen, Huinan Chen, Shengqu He, Cheng Jin, Zhicheng Hu and 7 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.3field-weighted citation impact, top 13% of its field
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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. FGF family in health and disease.Molecular biomedicine · 2026
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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

17 authors at 3 institutions in 1 country.

Yunjie Chen *School of Pharmaceutical Science, Wenzhou Medical University, 325000, Wenzhou, PR China.
Ning An *Department of Pharmacy, Ningbo Medical Center Lihuili Hospital, 315041, Ningbo, PR China.
Xuan Zhou *Department of Pharmacy, Ningbo first Hospital, 315010, Ningbo, PR China.
Lin Mei *School of Pharmaceutical Science, Wenzhou Medical University, 325000, Wenzhou, PR China.
Yanru SuiSchool of Pharmaceutical Science, Wenzhou Medical University, 325000, Wenzhou, PR China.
Gen ChenSchool of Pharmaceutical Science, Wenzhou Medical University, 325000, Wenzhou, PR China.
Huinan ChenSchool of Pharmaceutical Science, Wenzhou Medical University, 325000, Wenzhou, PR China.
Shengqu HeSchool of Pharmaceutical Science, Wenzhou Medical University, 325000, Wenzhou, PR China.
Cheng JinSchool of Pharmaceutical Science, Wenzhou Medical University, 325000, Wenzhou, PR China.
Zhicheng HuSchool of Pharmaceutical Science, Wenzhou Medical University, 325000, Wenzhou, PR China.
Wanqian LiSchool of Pharmaceutical Science, Wenzhou Medical University, 325000, Wenzhou, PR China.
Yang WangSchool of Pharmaceutical Science, Wenzhou Medical University, 325000, Wenzhou, PR China.
Zhu LinDepartment of Pharmacy, Ningbo first Hospital, 315010, Ningbo, PR China.
Peng ChenDepartment of Cardiology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325000, Wenzhou, PR China.
Litai JinSchool of Pharmaceutical Science, Wenzhou Medical University, 325000, Wenzhou, PR China. jin_litai@126.com.ORCID 0000-0002-7598-5938
Xueqiang GuanDepartment of Cardiology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325000, Wenzhou, PR China. wzsgxq@163.com.ORCID 0000-0001-5561-2440
Xu WangSchool of Pharmaceutical Science, Wenzhou Medical University, 325000, Wenzhou, PR China. wang_xu2003@163.com.ORCID 0000-0003-4781-5250
Wenzhou Medical University · CNNingbo First Hospital · CNNingbo Medical Center Lihuili Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac hypertrophy occurs initially in response to an increased cardiac load as a compensatory mechanism to maintain cardiac output. However, sustained pathological hypertrophy can develop into heart failure and cause sudden death. Fibroblast growth factor 20 (FGF20) is a member of the fibroblast growth factor family, which involved in apoptosis, aging, inflammation, and autophagy. The precise function of FGF20 in pathological cardiac hypertrophy is unclear. In this study, we demonstrated that FGF20 was significantly decreased in response to hypertrophic stimulation. In contrast, overexpression of FGF20 protected against pressure overload-induced cardiac hypertrophy. Mechanistically, we found that FGF20 upregulates SIRT1 expression, causing deacetylation of FOXO1; this effect promotes the transcription of downstream antioxidant genes, thus inhibits oxidative stress. In content, the anti-hypertrophic effect of FGF20 was largely counteracted in SIRT1-knockout mice, accompanied by an increase in oxidative stress. In summary, our findings reveal a previously unknown protective effect of FGF20 on pathological cardiac hypertrophy by reducing oxidative stress through activation of the SIRT1 signaling pathway. FGF20 is a potential novel molecular target for preventing and treating pressure overload-induced myocardial injury.

Indexed as

CardiomegalySirtuin 1AnimalsFibroblast Growth FactorsMiceMice, Inbred C57BLMice, KnockoutMyocytes, CardiacSignal TransductionFgf20 protein, mouseFibroblast Growth FactorsSirt1 protein, mouseSirtuin 1

Identifiers

PMID35351862
PMCPMC8964679
OpenAlexW4220816040

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.