Evidence map›Paper›PMID 25644112›Full record

ArticleJournal of the American Society of Nephrology : JASN2015

Regulation of Mitochondrial Dynamics by Dynamin-Related Protein-1 in Acute Cardiorenal Syndrome.

Maki Sumida, Kent Doi, Emi Ogasawara, Tetsushi Yamashita, Yoshifumi Hamasaki, Taro Kariya, Eiki Takimoto, Naoki Yahagi, Masaomi Nangaku, Eisei Noiri

Abstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 2 pooled it
3.9field-weighted citation impact, top 6% 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

72 citing papers in PubMed, 2 syntheses or guidelines pooled it, 125 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
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  5. Article
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  7. Article
  8. Article
  9. Article
  10. Acute kidney injury disrupts cardiac remodeling via SerpinA3N.bioRxiv : the preprint server for biology · 2025
    Article
  11. Review
  12. Review
  13. Article
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  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. New Insight in Cardiorenal Syndrome: From Biomarkers to Therapy.International journal of molecular sciences · 2023
    Review

12 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

10 authors at 4 institutions in 2 countries.

Maki SumidaDepartment of Nephrology and Endocrinology.
Kent DoiDepartment of Nephrology and Endocrinology, Department of Emergency and Critical Care Medicine, kdoi-tky@umin.ac.jp.
Emi OgasawaraDepartment of Nephrology and Endocrinology.
Tetsushi YamashitaDepartment of Nephrology and Endocrinology.
Yoshifumi HamasakiDepartment of Nephrology and Endocrinology, 22nd Century Medical and Research Center, and.
Taro KariyaDepartment of Cardiovascular Medicine, The University of Tokyo, Tokyo, Japan; and.
Eiki TakimotoDepartment of Cardiovascular Medicine, The University of Tokyo, Tokyo, Japan; and.
Naoki YahagiDepartment of Emergency and Critical Care Medicine.
Masaomi NangakuDepartment of Nephrology and Endocrinology.
Eisei NoiriDepartment of Nephrology and Endocrinology, Japan Science and Technology Agency/Japan International Cooperation Agency, Science and Technology Research Partnership for Sustainable Development, Tokyo, Japan.
The University of Tokyo · JPCentury Health · USJapan Science and Technology Agency · JPUniversity of Tokyo Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Experimental evidence has clarified distant organ dysfunctions induced by AKI. Crosstalk between the kidney and heart, which has been recognized recently as cardiorenal syndrome, appears to have an important role in clinical settings, but the mechanisms by which AKI causes cardiac injury remain poorly understood. Both the kidney and heart are highly energy-demanding organs that are rich in mitochondria. Therefore, we investigated the role of mitochondrial dynamics in kidney-heart organ crosstalk. Renal ischemia reperfusion (IR) injury was induced by bilateral renal artery clamping for 30 min in 8-week-old male C57BL/6 mice. Electron microscopy showed a significant increase of mitochondrial fragmentation in the heart at 24 h. Cardiomyocyte apoptosis and cardiac dysfunction, evaluated by echocardiography, were observed at 72 h. Among the mitochondrial dynamics regulating molecules, dynamin-related protein 1 (Drp1), which regulates fission, and mitofusin 1, mitofusin 2, and optic atrophy 1, which regulate fusion, only Drp1 was increased in the mitochondrial fraction of the heart. A Drp1 inhibitor, mdivi-1, administered before IR decreased mitochondrial fragmentation and cardiomyocyte apoptosis significantly and improved cardiac dysfunction induced by renal IR. This study showed that renal IR injury induced fragmentation of mitochondria in a fission-dominant manner with Drp1 activation and subsequent cardiomyocyte apoptosis in the heart. Furthermore, cardiac dysfunction induced by renal IR was improved by Drp1 inhibition. These data suggest that mitochondrial fragmentation by fission machinery may be a new therapeutic target in cardiac dysfunction induced by AKI.

Indexed as

Mitochondrial DynamicsAcute DiseaseAnimalsCardio-Renal SyndromeDynaminsMaleMiceMice, Inbred C57BLDnm1l protein, mouseDynaminsacute renal failureapoptosiscardiovascularmitochondria

Identifiers

PMID25644112
PMCPMC4587696
OpenAlexW2104965548

What OpenQuestion holds

Textmetadata
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.