Evidence map›Paper›PMID 40295524›Full record

ArticleNature communications2025

DNA damage in proximal tubules triggers systemic metabolic dysfunction through epigenetically altered macrophages.

Erina Sugita Nishimura, Akihito Hishikawa, Ran Nakamichi, Riki Akashio, Shunsuke Chikuma, Akinori Hashiguchi, Norifumi Yoshimoto, Eriko Yoshida Hama, Tomomi Maruki, Wataru Itoh and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
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

14 authors.

Erina Sugita Nishimura *Division of Nephrology, Endocrinology and Metabolism, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.
Akihito Hishikawa *Division of Nephrology, Endocrinology and Metabolism, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.
Ran Nakamichi *Division of Nephrology, Endocrinology and Metabolism, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.
Riki AkashioDivision of Nephrology, Endocrinology and Metabolism, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.
Shunsuke ChikumaDepartment of Immunology, Keio University School of Medicine, Tokyo, Japan.
Akinori HashiguchiDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.ORCID http://orcid.org/0000-0002-6455-071X
Norifumi YoshimotoDivision of Nephrology, Endocrinology and Metabolism, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.
Eriko Yoshida HamaDivision of Nephrology, Endocrinology and Metabolism, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.
Tomomi MarukiDivision of Nephrology, Endocrinology and Metabolism, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.
Wataru ItohDivision of Nephrology, Endocrinology and Metabolism, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.
Shintaro YamaguchiSchool of Medicine Medical Education Center, Keio University, Tokyo, Japan.ORCID http://orcid.org/0000-0002-4917-033X
Jun YoshinoDivision of Nephrology, Department of Internal Medicine, Faculty of Medicine, Shimane University, Izumo, Japan.
Hiroshi ItohCenter for Preventive Medicine, Keio University Hospital, Tokyo, Japan.
Kaori HayashiDivision of Nephrology, Endocrinology and Metabolism, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan. kaorihayashi@keio.jp.ORCID http://orcid.org/0000-0002-4923-1550

Funding

Japan Agency for Medical Research and Development (AMED) JP24gm6710029h0001
6 · The paper itself

Abstract

DNA damage repair is a critical physiological process closely linked to aging. The accumulation of DNA damage in renal proximal tubular epithelial cells (PTEC) is related to a decline in kidney function. Here, we report that DNA double-strand breaks in PTECs lead to systemic metabolic dysfunction, including weight loss, reduced fat mass, impaired glucose tolerance with mitochondrial dysfunction, and increased inflammation in adipose tissues and the liver. Single-cell RNA sequencing analysis reveals expansion of CD11c+ Ccr2+ macrophages in the kidney cortex, liver, and adipose tissues and Ly6C

Indexed as

DNA DamageEpigenesis, GeneticKidney Tubules, ProximalMacrophagesAdipose TissueAnimalsDNA Breaks, Double-StrandedDNA MethylationEpithelial CellsGasderminsIntracellular Signaling Peptides and ProteinsLiverMacrophage ActivationMaleMiceMice, Inbred C57BLGasderminsGsdmd protein, mouseIntracellular Signaling Peptides and ProteinsPhosphate-Binding Proteins

Identifiers

PMID40295524
PMCPMC12037803

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.