Evidence map›Paper›PMID 31655022›Full record

ArticleBritish journal of pharmacology2020

FOXO1 inhibition prevents renal ischemia-reperfusion injury via cAMP-response element binding protein/PPAR-γ coactivator-1α-mediated mitochondrial biogenesis.

Di Wang, Yanqing Wang, Xiantong Zou, Yundi Shi, Qian Liu, Tianru Huyan, Jing Su, Qi Wang, Fengxue Zhang, Xuejun Li and 1 more

Abstract read
In one paragraph

Article in British journal of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
–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

71 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  7. Mitophagy in kidney transplantation ischemia-reperfusion injury.International urology and nephrology · 2026
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11 more citing papers are in PubMed but not listed here.

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

11 authors.

Di WangState Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University and Beijing Key Laboratory of Tumor Systems Biology, Peking University, Beijing, China.ORCID 0000-0002-1847-7283
Yanqing WangState Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University and Beijing Key Laboratory of Tumor Systems Biology, Peking University, Beijing, China.
Xiantong ZouDepartment of Endocrinology and Metabolism, Peking University People's Hospital, Beijing, China.
Yundi ShiState Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University and Beijing Key Laboratory of Tumor Systems Biology, Peking University, Beijing, China.
Qian LiuState Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University and Beijing Key Laboratory of Tumor Systems Biology, Peking University, Beijing, China.
Tianru HuyanState Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University and Beijing Key Laboratory of Tumor Systems Biology, Peking University, Beijing, China.
Jing SuDepartment of Pathology, School of Basic Medical Sciences, Peking University, Beijing, China.
Qi WangInstitute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, Guangzhou, China.
Fengxue ZhangResearch Center of Integrative Medicine, School of Basic Medical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, China.
Xuejun LiState Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University and Beijing Key Laboratory of Tumor Systems Biology, Peking University, Beijing, China.
Lu TieState Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University and Beijing Key Laboratory of Tumor Systems Biology, Peking University, Beijing, China.ORCID 0000-0003-4755-2091

Funding

Beijing Golden Bridge Seed Capital Project ZZ16019Beijing Higher Education Young Elite Teacher Project YETP0053Beijing Natural Science Foundation 7172119Fund of Janssen Research Council China JRCC2011Leading Academic Discipline Project of Beijing Education Bureau BMU20110254National Natural Science Foundation of China 30901803National Natural Science Foundation of China 81373405National Natural Science Foundation of China 81473235National Natural Science Foundation of China 81673453National Natural Science Foundation of China 81673486National Natural Science Foundation of China 81874318National Natural Science Foundation of China 81974506
6 · The paper itself

Abstract

background and purposeGrowing evidence indicates targeting mitochondrial dynamics and biogenesis could accelerate recovery from renal ischemia-reperfusion (I/R) injury, but the underlying mechanisms remain elusive. Transcription factor forkhead box O1 (FOXO1) is a key regulator of mitochondrial homeostasis and plays a pathological role in the progression of renal disease. EXPERIMENTAL APPROACH: A mouse model of renal I/R injury and a hypoxia/reoxygenation (H/R) injury model for human renal tubular epithelial cells were used. KEY

resultsI/R injury up-regulated renal expression of FOXO1 and treatment with FOXO1-selective inhibitor AS1842856 prior to I/R injury decreased serum urea nitrogen, serum creatinine and the tubular damage score after injury. Post-I/R injury AS1842856 treatment could also ameliorate renal function and improve the survival rate of mice following injury. AS1842856 administration reduced mitochondrial-mediated apoptosis, suppressed the overproduction of mitochondrial ROS and accelerated recovery of ATP both in vivo and in vitro. Additionally, FOXO1 inhibition improved mitochondrial biogenesis and suppressed mitophagy. Expression of PPAR-γ coactivator 1α (PGC-1α), a master regulator of mitochondrial biogenesis, was down-regulated in both I/R and H/R injury, which could be abrogated by FOXO1 inhibition. Experiments using integrated bioinformatics analysis and coimmunoprecipitation established that FOXO1 inhibited PGC-1α transcription by competing with cAMP-response element binding protein (CREB) for its binding to transcriptional coactivators CREBBP/EP300 (CBP/P300). CONCLUSION AND IMPLICATIONS: These findings suggested that FOXO1 was critical to maintain mitochondrial function in renal tubular epithelial cells and FOXO1 may serve as a therapeutic target for pharmacological intervention in renal I/R injury.

Indexed as

Organelle BiogenesisAnimalsApoptosisCell LineCyclic AMP Response Element-Binding ProteinDisease Models, AnimalForkhead Box Protein O1HumansKidney DiseasesKidney TubulesMaleMice, Inbred C57BLMitochondriaMitophagyPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaQuinolones5-amino-7-(cyclohexylamino)-1-ethyl-6-fluoro-4-oxo-1,4-dihydroquinoline-3-carboxylic acidCREB1 protein, humanCreb1 protein, mouseCyclic AMP Response Element-Binding ProteinForkhead Box Protein O1FOXO1 protein, humanFoxo1 protein, mousePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanPpargc1a protein, mouseQuinolones

Identifiers

PMID31655022
PMCPMC6989953

What OpenQuestion holds

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Registered trials

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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.