Evidence map›Paper›PMID 38565675›Full record

ArticleCommunications biology2024

Deletion of podocyte Rho-associated, coiled-coil-containing protein kinase 2 protects mice from focal segmental glomerulosclerosis.

Keiichiro Matoba, Yosuke Nagai, Kensuke Sekiguchi, Shinji Ohashi, Etsuko Mitsuyoshi, Masayuki Shimoda, Toshiaki Tachibana, Daiji Kawanami, Tamotsu Yokota, Kazunori Utsunomiya and 1 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

7 citing papers in PubMed, 5 citations in OpenAlex.

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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 at 3 institutions in 1 country.

Keiichiro MatobaDivision of Diabetes, Metabolism and Endocrinology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, 105-8461, Japan. matoba@jikei.ac.jp.ORCID 0000-0003-0041-0483
Yosuke NagaiDivision of Diabetes, Metabolism and Endocrinology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, 105-8461, Japan.ORCID 0000-0001-8373-8147
Kensuke SekiguchiDivision of Diabetes, Metabolism and Endocrinology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, 105-8461, Japan.
Shinji OhashiDivision of Diabetes, Metabolism and Endocrinology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, 105-8461, Japan.
Etsuko MitsuyoshiDivision of Diabetes, Metabolism and Endocrinology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, 105-8461, Japan.
Masayuki ShimodaDepartment of Pathology, The Jikei University School of Medicine, Tokyo, 105-8461, Japan.
Toshiaki TachibanaCore Research Facilities for Basic Science, Research Center for Medical Science, The Jikei University School of Medicine, Tokyo, 105-8461, Japan.
Daiji KawanamiDepartment of Endocrinology and Diabetes, Fukuoka University School of Medicine, Fukuoka, 814-0180, Japan.ORCID 0000-0002-8926-4701
Tamotsu YokotaDivision of Diabetes, Metabolism and Endocrinology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, 105-8461, Japan.
Kazunori UtsunomiyaNomura Hospital, Tokyo, 181-8503, Japan.
Rimei NishimuraDivision of Diabetes, Metabolism and Endocrinology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, 105-8461, Japan.
Jikei University School of Medicine · JPFukuoka University · JPKawamura Hospital · JP

Funding

Astellas Foundation for Research on Metabolic Disorders N/AIchiro Kanehara Foundation for the Promotion of Medical Sciences and Medical Care (Ichiro Kanehara Foundation) N/AJapan Diabetes Society (JDS) N/AMEXT | Japan Society for the Promotion of Science (JSPS) 20K08645MEXT | Japan Society for the Promotion of Science (JSPS) 21K20914MEXT | Japan Society for the Promotion of Science (JSPS) 22K08347MEXT | Japan Society for the Promotion of Science (JSPS) 23K07709Mochida Memorial Foundation for Medical and Pharmaceutical Research N/A
6 · The paper itself

Abstract

Focal segmental glomerulosclerosis (FSGS) shares podocyte damage as an essential pathological finding. Several mechanisms underlying podocyte injury have been proposed, but many important questions remain. Rho-associated, coiled-coil-containing protein kinase 2 (ROCK2) is a serine/threonine kinase responsible for a wide array of cellular functions. We found that ROCK2 is activated in podocytes of adriamycin (ADR)-induced FSGS mice and cultured podocytes stimulated with ADR. Conditional knockout mice in which the ROCK2 gene was selectively disrupted in podocytes (PR2KO) were resistant to albuminuria, glomerular sclerosis, and podocyte damage induced by ADR injection. In addition, pharmacological intervention for ROCK2 significantly ameliorated podocyte loss and kidney sclerosis in a murine model of FSGS by abrogating profibrotic factors. RNA sequencing of podocytes treated with a ROCK2 inhibitor proved that ROCK2 is a cyclic nucleotide signaling pathway regulator. Our study highlights the potential utility of ROCK2 inhibition as a therapeutic option for FSGS.

Indexed as

Glomerulosclerosis, Focal SegmentalPodocytesAnimalsDoxorubicinMiceMice, KnockoutProtein Serine-Threonine Kinasesrho-Associated KinasesSclerosisDoxorubicinProtein Serine-Threonine Kinasesrho-Associated KinasesRock2 protein, mouse

Identifiers

PMID38565675
PMCPMC10987559
OpenAlexW4393409319

What OpenQuestion holds

Textmetadata
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.