Evidence map›Paper›PMID 42834985›Full record

ArticleiScience2026

RhoA through its various effectors mediate mitochondrial fragmentation in polycystic kidney disease.

Rohankrishna Harikumar, Zsuzsanna Lichner, Chen Tuo, Kuiru Wei, Ella Grieve, Rola M Saleeb, Andrew Wilde, Katalin Szászi, András Kapus

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Rohankrishna HarikumarKeenan Research Centre for Biomedical Science of the St. Michael's Hospital, University of Toronto, Toronto, ON M5B 1T8, Canada.
Zsuzsanna LichnerKeenan Research Centre for Biomedical Science of the St. Michael's Hospital, University of Toronto, Toronto, ON M5B 1T8, Canada.
Chen TuoKeenan Research Centre for Biomedical Science of the St. Michael's Hospital, University of Toronto, Toronto, ON M5B 1T8, Canada.
Kuiru WeiKeenan Research Centre for Biomedical Science of the St. Michael's Hospital, University of Toronto, Toronto, ON M5B 1T8, Canada.
Ella GrieveKeenan Research Centre for Biomedical Science of the St. Michael's Hospital, University of Toronto, Toronto, ON M5B 1T8, Canada.
Rola M SaleebKeenan Research Centre for Biomedical Science of the St. Michael's Hospital, University of Toronto, Toronto, ON M5B 1T8, Canada.
Andrew WildeDepartment Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON M5B 1T8, Canada.
Katalin SzásziKeenan Research Centre for Biomedical Science of the St. Michael's Hospital, University of Toronto, Toronto, ON M5B 1T8, Canada.
András KapusKeenan Research Centre for Biomedical Science of the St. Michael's Hospital, University of Toronto, Toronto, ON M5B 1T8, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Polycystic kidney disease (PKD), the most common genetic nephropathy, is caused by the loss/loss of function of polycystin-1 (PC1) or 2 (PC2) and characterized by cyst formation and fibrosis. A key feature of PKD is mitochondrial fragmentation, but the underlying mechanism is unknown. Since PC1/PC2 loss induces RhoA activation and fibrogenesis, we hypothesized that RhoA might also trigger general and/or PC1/2 loss-induced mitochondrial fragmentation. We show that RhoA activation is sufficient to induce DRP1-mediated mitochondrial fission in tubular cells. Importantly, genetic or pharmacologic inhibition of RhoA or its effectors (ROCK/LIM kinase/cofilin, phospho-myosin or formins) prevents/reverses PC1/PC2 loss-provoked fragmentation. Fragmentation by active formins requires F-actin polymerizing capacity but not binding to INF2, a RhoA-independent, fission-mediating formin. PC1 re-expression or RhoA/RhoA effector inhibition restores mitochondrial morphology in human PKD cells. Mitochondrial fragmentation facilitates fibrogenesis. Thus, RhoA regulates mitochondrial shape, and RhoA-mediated actin polymerization/myosin activation is a central mechanism of PKD-associated mitochondrial fragmentation.

Indexed as

actincytoskeletonDrp1fibrosisforminsmitochondrial fragmentationmyosinpolycystic kidney diseaseRhoA small GTPaseRho-signaling

Identifiers

PMID42834985
PMCPMC13634999

What OpenQuestion holds

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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.