Student or educator? Sign up with your school email and get 6 months of Pro free.
Cited by 711

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

TGF-ß Signaling in Renal Disease

Bo[Combining Diaeresis]ttinger, Erwin P., Bitzer, Markus·2002·Journal of the American Society of Nephrology

Abstract

Since discovery over a decade ago of a role for the cytokine TGF-beta as key mediator of glomerular and tubulointerstitial pathobiology in chronic kidney diseases, studies of TGF-beta signaling in the kidney have focused on the molecular biology of fibrogenesis. In recent years, glomerular and tubular epithelial cell apoptosis and cellular transdifferentiation have been proposed as putative primary pathomechanisms that may underlie progression of renal disease. This review describes evidence in support of nonlinear models and functional roles of TGF-beta signaling in mediating apoptosis and epithelial-to-mesenchymal transdifferentiation (EMT) in chronic progressive renal disease. Emphasis is placed on cell context-dependent models of TGF-beta signaling providing a conceptual framework to consolidate seemingly distinct pathomechanisms of progression of glomerular and tubulointerstitial disease.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1097/01.asn.0000033611.79556.ae

Cites

2 of 2 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 2 references

Cited by

See all 711

Metadata

Authors
Bo[Combining Diaeresis]ttinger, E. P., & Bitzer, M.
Venue
Journal of the American Society of Nephrology
Published
2002-10
Volume
13
Issue
10
Pages
2600-2610
ISSN
1046-6673 (ISSN-L)
OpenAlex
W2132803823
Cited by
711
References
2
FWCI
8.96
Type
journal article
Language
en
Open access
closed

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

How to cite

Cite CoChat for the checks on this page, and the paper for its own findings.

This page
CoChat. (2026). Citation check: TGF-ß Signaling in Renal Disease. https://app.cochat.ai/papers/10.1097/01.asn.0000033611.79556.ae
The paper
Bo[Combining Diaeresis]ttinger, E. P., & Bitzer, M. (2002). TGF-ß Signaling in Renal Disease. Journal of the American Society of Nephrology. https://doi.org/10.1097/01.asn.0000033611.79556.ae

Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.