Evidence map›Paper›PMID 35902687›Full record

ArticleCommunications biology2022

Mesenchymal stem cells exert renoprotection via extracellular vesicle-mediated modulation of M2 macrophages and spleen-kidney network.

Yuko Shimamura, Kazuhiro Furuhashi, Akihito Tanaka, Munetoshi Karasawa, Tomoya Nozaki, Shintaro Komatsu, Kenshi Watanabe, Asuka Shimizu, Shun Minatoguchi, Makoto Matsuyama and 5 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 16 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

15 authors at 3 institutions in 1 country.

Yuko Shimamura *Department of Nephrology, Internal Medicine, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya, Aichi, Japan.
Kazuhiro Furuhashi *Department of Nephrology, Internal Medicine, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya, Aichi, Japan. furu13@med.nagoya-u.ac.jp.ORCID 0000-0003-2476-688X
Akihito Tanaka *Department of Nephrology, Internal Medicine, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya, Aichi, Japan.
Munetoshi KarasawaDepartment of Nephrology, Internal Medicine, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya, Aichi, Japan.
Tomoya NozakiDepartment of Nephrology, Internal Medicine, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya, Aichi, Japan.
Shintaro KomatsuDepartment of Nephrology, Internal Medicine, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya, Aichi, Japan.
Kenshi WatanabeDepartment of Nephrology, Internal Medicine, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya, Aichi, Japan.
Asuka ShimizuDepartment of Nephrology, Internal Medicine, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya, Aichi, Japan.
Shun MinatoguchiDepartment of Nephrology, Internal Medicine, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya, Aichi, Japan.
Makoto MatsuyamaDivision of Molecular Genetics, Shigei Medical Research Institute, Minami-ku, Okayama, Japan.ORCID 0000-0003-2606-059X
Yuriko SawaDepartment of Nephrology, Internal Medicine, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya, Aichi, Japan.
Naotake TsuboiDepartment of Nephrology, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.
Takuji IshimotoDepartment of Nephrology, Internal Medicine, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya, Aichi, Japan.
Hiroshi I SuzukiDivision of Molecular Oncology, Center for Neurological Diseases and Cancer, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya, Aichi, Japan.ORCID 0000-0003-4682-5086
Shoichi MaruyamaDepartment of Nephrology, Internal Medicine, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya, Aichi, Japan.ORCID 0000-0002-8858-632X
Nagoya University · JPFujita Health University · JPShigei Medical Research Institute · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adipose-derived mesenchymal stem cells (ASCs) have shown therapeutic potentials against refractory diseases. However, the detailed therapeutic mechanisms remain unclear. Here, we report the therapeutic actions of human ASCs in nephritis, focusing on cellular dynamics and multi-organ networks. Intravenously-administered ASCs accumulated in spleen but not kidneys. Nevertheless, ASCs increased M2 macrophages and Tregs in kidneys and drove strong renoprotection. Splenectomy abolished these therapeutic effects. ASC-derived extracellular vesicles (EVs) were transferred to M2 macrophages, which entered the bloodstream from spleen. EVs induced the transcriptomic signatures of hyperpolarization and PGE2 stimulation in M2 macrophages and ameliorated glomerulonephritis. ASCs, ASC-derived EVs, and EV-transferred M2 macrophages enhanced Treg induction. These findings suggest that EV transfer from spleen-accumulated ASCs to M2 macrophages and subsequent modulation of renal immune-environment underlie the renoprotective effects of ASCs. Our results provide insights into the therapeutic actions of ASCs, focusing on EV-mediated modulation of macrophages and the spleen-kidney immune network.

Indexed as

Extracellular VesiclesMesenchymal Stem CellsHumansMacrophagesSpleenT-Lymphocytes, Regulatory

Identifiers

PMID35902687
PMCPMC9334610
OpenAlexW4288080409

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.