Evidence map›Paper›PMID 30532765›Full record

ArticleFrontiers in genetics2018

FGF10 Protects Against Renal Ischemia/Reperfusion Injury by Regulating Autophagy and Inflammatory Signaling.

Xiaohua Tan, Hongmei Zhu, Qianyu Tao, Lisha Guo, Tianfang Jiang, Le Xu, Ruo Yang, Xiayu Wei, Jin Wu, Xiaokun Li and 1 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Frontiers in genetics, 2018. 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 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

30 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
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  4. High-mobility group box 1 in acute kidney injury.Frontiers in pharmacology · 2025
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Xiaohua TanSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Hongmei ZhuSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Qianyu TaoSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Lisha GuoSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Tianfang JiangThe First Affiliated Hospital, Wenzhou Medical University, Wenzhou, China.
Le XuThe First Affiliated Hospital, Wenzhou Medical University, Wenzhou, China.
Ruo YangSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Xiayu WeiInstitute of Life Sciences, Wenzhou University, Wenzhou, China.
Jin WuInstitute of Life Sciences, Wenzhou University, Wenzhou, China.
Xiaokun LiSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Jin-San ZhangSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Wenzhou Medical University · CNWenzhou University · CNFirst Affiliated Hospital of Wenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemia-reperfusion (I/R) is a common cause of acute kidney injury (AKI), which is associated with high mortality and poor outcomes. Autophagy plays important roles in the homeostasis of renal tubular cells (RTCs) and is implicated in the pathogenesis of AKI, although its role in the process is complex and controversial. Fibroblast growth factor 10 (FGF10), a multifunctional FGF family member, was reported to exert protective effect against cerebral ischemia injury and myocardial damage. Whether FGF10 has similar beneficial effect, and if so whether autophagy is associated with the potential protective activity against AKI has not been investigated. Herein, we report that FGF10 treatment improved renal function and histological integrity in a rat model of renal I/R injury. We observed that FGF10 efficiently reduced I/R-induced elevation in blood urea nitrogen, serum creatinine as well as apoptosis induction of RTCs. Interestingly, autophagy activation following I/R was suppressed by FGF10 treatment based on the immunohistochemistry staining and immunoblot analyses of LC3, Beclin-1 and SQSTM1/p62. Moreover, combined treatment of FGF10 with Rapamycin partially reversed the renoprotective effect of FGF10 suggesting the involvement of mTOR pathway in the process. Interestingly, FGF10 also inhibited the release of HMGB1 from the nucleus to the extracellular domain and regulated the expression of inflammatory cytokines such as TNF-α, IL-1β and IL-6. Together, these results indicate that FGF10 could alleviate kidney I/R injury by suppressing excessive autophagy and inhibiting inflammatory response and may therefore have the potential to be used for the prevention and perhaps treatment of I/R-associated AKI.

Indexed as

acute kidney injuryautophagyFGF10HMGB1inflammationischemia-reperfusion

Identifiers

PMID30532765
PMCPMC6265307
OpenAlexW2901101732

What OpenQuestion holds

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LicenceCC BY
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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.