The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index.
The actin cytoskeleton of kidney podocytes is a direct target of the antiproteinuric effect of cyclosporine A
Open accessAbstract
The immunosuppressive action of the calcineurin inhibitor cyclosporine A (CsA) stems from the inhibition of nuclear factor of activated T cells (NFAT) signaling in T cells. CsA is also used for the treatment of proteinuric kidney diseases. As it stands, the antiproteinuric effect of CsA is attributed to its immunosuppressive action. Here we show that the beneficial effect of CsA on proteinuria is not dependent on NFAT inhibition in T cells, but rather results from the stabilization of the actin cytoskeleton in kidney podocytes. CsA blocks the calcineurin-mediated dephosphorylation of synaptopodin, a regulator of Rho GTPases in podocytes, thereby preserving the phosphorylation-dependent synaptopodin–14-3-3β interaction. Preservation of this interaction, in turn, protects synaptopodin from cathepsin L–mediated degradation. These results represent a new view of calcineurin signaling and shed further light on the treatment of proteinuric kidney diseases. Novel calcineurin substrates such as synaptopodin may provide promising starting points for antiproteinuric drugs that avoid the serious side effects of long-term CsA treatment.
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.
Integrity signals
Registry
Cites
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.
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
A severe combined immunodeficiency mutation in the mouse
Bosma, G. C., Custer, R. P., & Bosma, M. J. (1983) · Nature · doi:10.1038/301527a0 · Cited by 2,207
The Structural Basis for 14-3-3:Phosphopeptide Binding Specificity
Yaffe, M. B., Rittinger, K., Volinia, S., Caron, P. R., Aitken, A., Leffers, H., Gamblin, S. J., Smerdon, S. J., & Cantley, L. C. (1997) · Cell · doi:10.1016/s0092-8674(00)80487-0 · Cited by 1,604
14-3-3 Proteins: Structure, Function, and Regulation
Fu, H., Subramanian, R. R., & Masters, S. C. (2000) · Annual Review of Pharmacology and Toxicology · doi:10.1146/annurev.pharmtox.40.1.617 · Cited by 1,579
Immunosuppressive Drugs for Kidney Transplantation
Halloran, P. F. (2004) · New England Journal of Medicine · doi:10.1056/nejmra033540 · Cited by 1,555
Interaction of 14-3-3 with Signaling Proteins Is Mediated by the Recognition of Phosphoserine
Muslin, A. J., Tanner, J. W., Allen, P. M., & Shaw, A. S. (1996) · Cell · doi:10.1016/s0092-8674(00)81067-3 · Cited by 1,381
Crabtree, G. R., & Olson, E. N. (2002) · Cell · doi:10.1016/s0092-8674(02)00699-2 · Cited by 1,323
A Mutation in the TRPC6 Cation Channel Causes Familial Focal Segmental Glomerulosclerosis
Winn, M. P., Conlon, P. J., Lynn, K. L., Farrington, M. K., Creazzo, T., Hawkins, A. F., Daskalakis, N., Kwan, S. Y., Ebersviller, S., Burchette, J. L., et al. (2005) · Science · doi:10.1126/science.1106215 · Cited by 1,104
TRPC6 is a glomerular slit diaphragm-associated channel required for normal renal function
Reiser, J., Polu, K. R., Möller, C. C., Kenlan, P., Altintas, M. M., Wei, C., Faul, C., Herbert, S., Villegas, I., Avila-Casado, C., et al. (2005) · Nature Genetics · doi:10.1038/ng1592 · Cited by 863
Self-citationFK-506- and CsA-sensitive activation of the interleukin-2 promoter by calcineurin
O'Keefe, S. J., Tamura, J., Kincaid, R. L., Tocci, M. J., & O'Neill, E. A. (1992) · Nature · doi:10.1038/357692a0 · Cited by 841
How do 14‐3‐3 proteins work? – Gatekeeper phosphorylation and the molecular anvil hypothesis
Yaffe, M. B. (2002) · FEBS Letters · doi:10.1016/s0014-5793(01)03288-4 · Cited by 660
Cited by
FGF23 induces left ventricular hypertrophy
Faul, C., Amaral, A. P., Oskouei, B., Hu, M.-C., Sloan, A., Isakova, T., Gutiérrez, O. M., Aguillon-Prada, R., Lincoln, J., Hare, J. M., et al. (2011) · Journal of Clinical Investigation · doi:10.1172/jci46122 · Cited by 2,027
Self-citationSpecialized roles for cysteine cathepsins in health and disease
Reiser, J., Adair, B., & Reinheckel, T. (2010) · Journal of Clinical Investigation · doi:10.1172/jci42918 · Cited by 580
Self-citationThe podocyte slit diaphragm--from a thin grey line to a complex signalling hub
Grahammer, F., Schell, C., & Huber, T. B. (2013) · Nature Reviews Nephrology · doi:10.1038/nrneph.2013.169 · Cited by 269
Adverse events associated with mTOR inhibitors
Pallet, N., & Legendre, C. (2013) · Expert Opinion on Drug Safety · doi:10.1517/14740338.2013.752814 · Cited by 198
Cathepsin D in Podocytes Is Important in the Pathogenesis of Proteinuria and CKD
Yamamoto-Nonaka, K., Koike, M., Asanuma, K., Takagi, M., Oliva Trejo, J. A., Seki, T., Hidaka, T., Ichimura, K., Sakai, T., Tada, N., et al. (2016) · Journal of the American Society of Nephrology · doi:10.1681/asn.2015040366 · Cited by 59
Advances in slit diaphragm signaling
New, L. A., Martin, C. E., & Jones, N. (2014) · Current Opinion in Nephrology and Hypertension · doi:10.1097/01.mnh.0000447018.28852.b6 · Cited by 45
Signal regulatory protein α protects podocytes through promotion of autophagic activity
Li, L., Liu, Y., Li, S., Yang, R., Zeng, C., Rong, W., Liang, H., Zhang, M., Zhu, X., Kidder, K., et al. (2019) · JCI Insight · doi:10.1172/jci.insight.124747 · Cited by 19
Hirashima, H., Komiya, T., Toriu, N., Hara, S., Matsunaga, A., Saito, T., & Muso, E. (2018) · Clinical Nephrology – Case Studies · doi:10.5414/cncs109509 · Cited by 8
Jehn, U., Schütte-Nütgen, K., Henke, U., Pavenstädt, H., Suwelack, B., & Reuter, S. (2021) · Scientific Reports · doi:10.1038/s41598-021-83333-7 · Cited by 6
Metadata
- Authors
- Faul, C., Donnelly, M., Merscher-Gomez, S., Chang, Y. H., Franz, S., Delfgaauw, J., Chang, J.-M., Choi, H. Y., Campbell, K. N., Kim, K., Reiser, J., & Mundel, P.
- Venue
- Nature Medicine
- Published
- 2008-08-24
- Volume
- 14
- Issue
- 9
- Pages
- 931-938
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W2144479843
- Cited by
- 991
- References
- 42
- FWCI
- 38.88
- Type
- journal article
- Language
- en
- Open access
- green
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
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.
