Evidence map›Paper›PMID 28687864›Full record

ReviewPflugers Archiv : European journal of physiology2017

Stressed podocytes-mechanical forces, sensors, signaling and response.

Karlhans Endlich, Felix Kliewe, Nicole Endlich

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pflugers Archiv : European journal of physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

52 citing papers in PubMed, 98 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Piezo1 and podocyte mechano-sensing in hypertensive nephropathy.Hypertension research : official journal of the Japanese Society of Hypertension · 2026
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Piezo1, F-Actin Remodeling, and Podocyte Survival and Regeneration.Journal of the American Society of Nephrology : JASN · 2025
    Article
  14. Article
  15. Article
  16. PIEZO1-Mediated Calcium Signaling and Podocyte Injury in Diabetic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2025
    Article
  17. Article
  18. Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Karlhans EndlichDepartment of Anatomy and Cell Biology, University Medicine Greifswald, 17489, Greifswald, Germany. karlhans.endlich@uni-greifswald.de.ORCID http://orcid.org/0000-0001-6052-6061
Felix KlieweDepartment of Anatomy and Cell Biology, University Medicine Greifswald, 17489, Greifswald, Germany.
Nicole EndlichDepartment of Anatomy and Cell Biology, University Medicine Greifswald, 17489, Greifswald, Germany.
Universitätsmedizin Greifswald · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increased glomerular capillary pressure (glomerular hypertension) and increased glomerular filtration rate (glomerular hyperfiltration) have been proven to cause glomerulosclerosis in animal models and are likely to be operative in patients. Since podocytes cover the glomerular basement membrane, they are exposed to tensile stress due to circumferential wall tension and to fluid shear stress arising from filtrate flow through the narrow filtration slits and through Bowman's space. In vitro evidence documents that podocytes respond to tensile stress as well as to fluid shear stress. Several proteins are discussed in this review that are expressed in podocytes and could act as mechanosensors converting mechanical force via a conformational change into a biochemical signal. The cation channels P2X4 and TRPC6 were shown to be involved in mechanosignaling in podocytes. P2X4 is activated by stretch-induced ATP release, while TRPC6 might be inherently mechanosensitive. Membrane, slit diaphragm and cell-matrix contact proteins are connected to the sublemmal actin network in podocytes via various linker proteins. Therefore, actin-associated proteins, like the proven mechanosensor filamin, are ideal candidates to sense forces in the podocyte cytoskeleton. Furthermore, podocytes express talin, p130Cas, and fibronectin that are known to undergo a conformational change in response to mechanical force exposing cryptic binding sites. Downstream of mechanosensors, experimental evidence suggests the involvement of MAP kinases, Ca

Indexed as

Mechanotransduction, CellularActin CytoskeletonAnimalsExtracellular MatrixGlomerulonephritisHumansIon ChannelsPodocytesSclerosisStress, MechanicalIon ChannelsChronic kidney diseaseGlomerulopathyMechanical stressMechanotransductionPodocyteStretch

Identifiers

PMID28687864
OpenAlexW2724183530

What OpenQuestion holds

Textmetadata
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.