Evidence map›Paper›PMID 33188449›Full record

ReviewPediatric nephrology (Berlin, Germany)2021

Role of actin cytoskeleton in podocytes.

Sanja Sever

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Pediatric nephrology (Berlin, Germany), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05875454 (Assessment of Podocyts Integrity in Glomerular Diseases.), which is not on this map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 17% 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.

NCT05875454 unknown statusnot on this mapstarted 2023, after this paper: background citation

Assessment of Podocyts Integrity in Glomerular Diseases.

TypeobservationalSponsorAssiut UniversityRan2023 to 2025Enrolled50ConditionsGlomerular DiseaseArmsHistopathological examination of tru-cut needle biopsy
3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Podocytopathies.Nature reviews. Disease primers · 2025
    Review
  8. Article
  9. Review
  10. Article
  11. Actin cytoskeleton and associated myosin motors within the renal epithelium.American journal of physiology. Renal physiology · 2024
    Review
  12. Minimal Change Disease: Pathogenetic Insights from Glomerular Proteomics.International journal of molecular sciences · 2024
    Article
  13. Article
  14. Store-operated CaExperimental biology and medicine (Maywood, N.J.) · 2023
    Review
  15. Roles of the cytoskeleton in human diseases.Molecular biology reports · 2023
    Review
  16. Review
  17. Review
  18. MRTF: Basic Biology and Role in Kidney Disease.International journal of molecular sciences · 2021
    Review
  19. Effect of tacrolimus on the expression of Park7 in glomerular podocytes injured by puromycin aminonucleoside.Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
    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

1 author at 1 institution in 1 country.

Sanja SeverHarvard Medical School and Massachusetts General Hospital, Boston, MA, USA. ssever@mgh.harvard.edu.
Harvard University · US

Funding

Use of small molecules that stabilize dynamin rings in podocytopathiesR01DK087985 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI SEVER, SANJA · 2011 to 2020
$3.4M
Role of dynamin for podocytes structure and functionR01DK093773 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI SEVER, SANJA · 2011 to 2021
$3.4M
NIDDK NIH HHS R01 DK087985NIDDK NIH HHS R01 DK093773
6 · The paper itself

Abstract

The selectivity of the glomerular filter is established by physical, chemical, and signaling interplay among its three core constituents: glomerular endothelial cells, the glomerular basement membrane, and podocytes. Functional impairment or injury of any of these three components can lead to proteinuria. Podocytes are injured in many forms of human and experimental glomerular disease, including minimal change disease, focal segmental glomerulosclerosis, and diabetes mellitus. One of the earliest signs of podocyte injury is loss of their distinct structure, which is driven by dysregulated dynamics of the actin cytoskeleton. The status of the actin cytoskeleton in podocytes depends on a set of actin binding proteins, nucleators and inhibitors of actin polymerization, and regulatory GTPases. Mutations that alter protein function in each category have been implicated in glomerular diseases in humans and animal models. In addition, a growing body of studies suggest that pharmacological modifications of the actin cytoskeleton have the potential to become novel therapeutics for podocyte-dependent chronic kidney diseases. This review presents an overview of the essential proteins that establish actin cytoskeleton in podocytes and studies demonstrating the feasibility of drugging actin cytoskeleton in kidney diseases.

Indexed as

Actin CytoskeletonPodocytesAnimalsHumansActin binding proteins (ABPs)Actin cytoskeletonGlomerular diseasesNucleators of actin polymerizationPodocytesRegulatory GTPases

Identifiers

PMID33188449
PMCPMC8116355
OpenAlexW3099792152

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.