Evidence map›Paper›PMID 32938919›Full record

ArticleNature communications2020

IRF1-mediated downregulation of PGC1α contributes to cardiorenal syndrome type 4.

Yinghui Huang, Shaobo Wang, Jie Zhou, Yong Liu, Changhong Du, Ke Yang, Xianjin Bi, Mingying Liu, Wenhao Han, Kailong Wang and 9 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

40 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Roles of microRNAs in cardiorenal syndrome.Molecular and cellular biochemistry · 2025
    Review
  8. Development of a Mouse Model of Uremic Cardiomyopathy: Investigating the Impact of Chronic Kidney Disease on Cardiac Function and Signaling Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  9. Review
  10. Colonization withbioRxiv : the preprint server for biology · 2025
    Article
  11. Article
  12. Article
  13. Review
  14. In chronic kidney disease altered cardiac metabolism precedes cardiac hypertrophy.American journal of physiology. Renal physiology · 2024
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Interferons and interferon-related pathways in heart disease.Frontiers in cardiovascular medicine · 2024
    Review
  20. Article
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

19 authors at 2 institutions in 1 country.

Yinghui HuangDepartment of Nephrology, The Key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), 400037, Chongqing, China.
Shaobo WangDepartment of Nephrology, The Key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), 400037, Chongqing, China.
Jie ZhouDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Army Medical University, 400038, Chongqing, China.
Yong LiuDepartment of Nephrology, The Key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), 400037, Chongqing, China.
Changhong DuInstitute of Combined Injury, State Key Laboratory of Trauma, Burns and Combined Injury, Chongqing Engineering Research Center for Nanomedicine, College of Preventive Medicine, Army Medical University, 400038, Chongqing, China.
Ke YangDepartment of Nephrology, The Key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), 400037, Chongqing, China.
Xianjin BiDepartment of Nephrology, The Key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), 400037, Chongqing, China.
Mingying LiuDepartment of Nephrology, The Key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), 400037, Chongqing, China.
Wenhao HanDepartment of Nephrology, The Key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), 400037, Chongqing, China.
Kailong WangDepartment of Nephrology, The Key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), 400037, Chongqing, China.
Jiachuan XiongDepartment of Nephrology, The Key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), 400037, Chongqing, China.
Song WangInstitute of Combined Injury, State Key Laboratory of Trauma, Burns and Combined Injury, Chongqing Engineering Research Center for Nanomedicine, College of Preventive Medicine, Army Medical University, 400038, Chongqing, China.
Yue WangDepartment of Nephrology, The Key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), 400037, Chongqing, China.
Ling NieDepartment of Nephrology, The Key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), 400037, Chongqing, China.
Chi LiuDepartment of Nephrology, The Key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), 400037, Chongqing, China.
Daohai ZhangDepartment of Nephrology, The Key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), 400037, Chongqing, China.
Jun GuState Key Laboratory of Protein and Plant Gene Research, College of Life Science, Peking University, 100871, Beijing, China.
Chunyu ZengDepartment of Cardiology, Daping Hospital, Army Medical University, 400042, Chongqing, China.ORCID http://orcid.org/0000-0003-0173-5028
Jinghong ZhaoDepartment of Nephrology, The Key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), 400037, Chongqing, China. zhaojh@tmmu.edu.cn.ORCID http://orcid.org/0000-0001-9750-3285
Army Medical University · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiorenal syndrome type 4 (CRS4) is a common complication of chronic kidney disease (CKD), but the pathogenic mechanisms remain elusive. Here we report that morphological and functional changes in myocardial mitochondria are observed in CKD mice, especially decreases in oxidative phosphorylation and fatty acid metabolism. High phosphate (HP), a hallmark of CKD, contributes to myocardial energy metabolism dysfunction by downregulating peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC1α). Furthermore, the transcriptional factor interferon regulatory factor 1 (IRF1) is revealed as the key molecule upregulated by HP through histone H3K9 acetylation, and responsible for the HP-mediated transcriptional inhibition of PGC1α by directly binding to its promoter region. Conversely, restoration of PGC1α expression or genetic knockdown of IRF1 significantly attenuates HP-induced alterations in vitro and in vivo. These findings demonstrate that IRF1-PGC1α axis-mediated myocardial energy metabolism remodeling plays a crucial role in the pathogenesis of CRS4.

Indexed as

AdolescentAdultAgedAged, 80 and overAnimalsCardio-Renal SyndromeDisease Models, AnimalDown-RegulationEnergy MetabolismGene Knockdown TechniquesGlomerular Filtration RateGlucuronidaseHeart FailureHumansInterferon Regulatory Factor-1Klotho ProteinsGlucuronidaseInterferon Regulatory Factor-1Irf1 protein, mouseKlotho ProteinsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPhosphatesPpargc1a protein, mouse

Identifiers

PMID32938919
PMCPMC7494935
OpenAlexW3087419449

What OpenQuestion holds

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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.