Evidence map›Paper›PMID 39261560›Full record

ArticleScientific reports2024

Deletion of p38 MAPK in macrophages ameliorates peritoneal fibrosis and inflammation in peritoneal dialysis.

Akie Ikushima, Takuya Ishimura, Keita P Mori, Hiroyuki Yamada, Sayaka Sugioka, Akira Ishii, Naohiro Toda, Shoko Ohno, Yukiko Kato, Takaya Handa and 2 more

Abstract read
In one paragraph

Article in Scientific reports, 2024. 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. Review
  2. Article
  3. Article
  4. 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

12 authors.

Akie IkushimaDepartment of Nephrology, Graduate School of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, Kyoto, 6068507, Japan.
Takuya IshimuraDepartment of Nephrology, Graduate School of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, Kyoto, 6068507, Japan.
Keita P MoriDepartment of Nephrology, Graduate School of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, Kyoto, 6068507, Japan.
Hiroyuki YamadaDepartment of Nephrology, Graduate School of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, Kyoto, 6068507, Japan.
Sayaka SugiokaDepartment of Nephrology, Graduate School of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, Kyoto, 6068507, Japan.
Akira IshiiDepartment of Nephrology, Graduate School of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, Kyoto, 6068507, Japan.
Naohiro TodaDepartment of Nephrology, Graduate School of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, Kyoto, 6068507, Japan.
Shoko OhnoDepartment of Nephrology, Graduate School of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, Kyoto, 6068507, Japan.
Yukiko KatoDepartment of Nephrology, Graduate School of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, Kyoto, 6068507, Japan.
Takaya HandaDepartment of Nephrology, Graduate School of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, Kyoto, 6068507, Japan.
Motoko YanagitaDepartment of Nephrology, Graduate School of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, Kyoto, 6068507, Japan.
Hideki YokoiDepartment of Nephrology, Graduate School of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, Kyoto, 6068507, Japan. yokoih@kuhp.kyoto-u.ac.jp.

Funding

Japan Agency for Medical Research and Development 19gm1210009Japan Society for the Promotion of Science 21K16189Japan Society for the Promotion of Science 22K08310Japan Society for the Promotion of Science 23K07717Japan Society for the Promotion of Science 23K15226Japan Society for the Promotion of Science 23K15227Japan Society for the Promotion of Science 24K19129
6 · The paper itself

Abstract

One of the most common causes of peritoneal dialysis withdrawal is ultrafiltration failure which is characterized by peritoneal membrane thickening and fibrosis. Although previous studies have demonstrated the inhibitory effect of p38 MAPK inhibitors on peritoneal fibrosis in mice, it was unclear which specific cells contribute to peritoneal fibrosis. To investigate the role of p38 MAPK in peritoneal fibrosis more precisely, we examined the expression of p38 MAPK in human peritoneum and generated systemic inducible p38 MAPK knockout mice and macrophage-specific p38 MAPK knockout mice. Furthermore, the response to lipopolysaccharide (LPS) was assessed in p38 MAPK-knocked down RAW 264.7 cells to further explore the role of p38 MAPK in macrophages. We found that phosphorylated p38 MAPK levels were increased in the thickened peritoneum of both human and mice. Both chlorhexidine gluconate (CG)-treated systemic inducible and macrophage-specific p38 MAPK knockout mice ameliorated peritoneal thickening, mRNA expression related to inflammation and fibrosis, and the number of αSMA- and MAC-2-positive cells in the peritoneum compared to CG control mice. Reduction of p38 MAPK in RAW 264.7 cells suppressed inflammatory mRNA expression induced by LPS. These findings suggest that p38 MAPK in macrophages plays a critical role in peritoneal inflammation and thickening.

Indexed as

InflammationMacrophagesp38 Mitogen-Activated Protein KinasesPeritoneal DialysisPeritoneal FibrosisAnimalsChlorhexidineHumansLipopolysaccharidesMaleMiceMice, KnockoutPeritoneumRAW 264.7 CellsChlorhexidinechlorhexidine gluconateLipopolysaccharidesp38 Mitogen-Activated Protein KinasesFibrosisMacrophagep38 MAPKPeritoneal dialysis

Identifiers

PMID39261560
PMCPMC11391064

What OpenQuestion holds

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Read underepoch 390

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.