Student or educator? Sign up with your school email and get 6 months of Pro free.
Cited by 181

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Defective podocyte insulin signalling through p85-XBP1 promotes ATF6-dependent maladaptive ER-stress response in diabetic nephropathy

Open access
Madhusudhan, Thati, Wang, Hongjie, Dong, Wei, Ghosh, Sanchita, Bock, Fabian, Thangapandi, Veera Raghavan, Ranjan, Satish, Wolter, Juliane, Kohli, Shrey, Shahzad, Khurrum, Heidel, Florian, Krueger, Martin, Schwenger, Vedat, Moeller, Marcus J., Kalinski, Thomas, Reiser, Jochen, Chavakis, Triantafyllos, Isermann, Berend·2015·Nature Communications

Abstract

Endoplasmic reticulum (ER) stress is associated with diabetic nephropathy (DN), but its pathophysiological relevance and the mechanisms that compromise adaptive ER signalling in podocytes remain unknown. Here we show that nuclear translocation of the transcription factor spliced X-box binding protein-1 (sXBP1) is selectively impaired in DN, inducing activating transcription factor-6 (ATF6) and C/EBP homology protein (CHOP). Podocyte-specific genetic ablation of XBP1 or inducible expression of ATF6 in mice aggravates DN. sXBP1 lies downstream of insulin signalling and attenuating podocyte insulin signalling by genetic ablation of the insulin receptor or the regulatory subunits phosphatidylinositol 3-kinase (PI3K) p85α or p85β impairs sXBP1 nuclear translocation and exacerbates DN. Corroborating our findings from murine DN, the interaction of sXBP1 with p85α and p85β is markedly impaired in the glomerular compartment of human DN. Thus, signalling via the insulin receptor, p85, and XBP1 maintains podocyte homeostasis, while disruption of this pathway impairs podocyte function in DN.

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 · 10.1038/ncomms7496

Cites

3 of 3 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 3 references

Cited by

See all 181

Metadata

Authors
Madhusudhan, T., Wang, H., Dong, W., Ghosh, S., Bock, F., Thangapandi, V. R., Ranjan, S., Wolter, J., Kohli, S., Shahzad, K., Heidel, F., Krueger, M., Schwenger, V., Moeller, M. J., Kalinski, T., Reiser, J., Chavakis, T., & Isermann, B.
Venue
Nature Communications
Published
2015-03-10
Volume
6
Issue
1
Pages
6496-6496
ISSN
2041-1723 (ISSN-L)
OpenAlex
W1976496691
Cited by
181
References
3
FWCI
7.40
Type
journal article
Language
en
Open access
gold

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: Defective podocyte insulin signalling through p85-XBP1 promotes ATF6-dependent maladaptive ER-stress response in diabetic nephropathy. https://app.cochat.ai/papers/10.1038/ncomms7496
The paper
Madhusudhan, T., Wang, H., Dong, W., Ghosh, S., Bock, F., Thangapandi, V. R., Ranjan, S., Wolter, J., Kohli, S., Shahzad, K., Heidel, F., Krueger, M., Schwenger, V., Moeller, M. J., Kalinski, T., Reiser, J., Chavakis, T., & Isermann, B. (2015). Defective podocyte insulin signalling through p85-XBP1 promotes ATF6-dependent maladaptive ER-stress response in diabetic nephropathy. Nature Communications. https://doi.org/10.1038/ncomms7496

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.