The DOI matches its Crossref record; 142 of the 142 references it cites were found in a registry or an index.
Molecular mechanisms and therapeutic targets for diabetic kidney disease
Open accessAbstract
Diabetic kidney disease has a high global disease burden and substantially increases the risk of kidney failure and cardiovascular events. Despite treatment, there is substantial residual risk of disease progression with existing therapies. Therefore, there is an urgent need to better understand the molecular mechanisms driving diabetic kidney disease to help identify new therapies that slow progression and reduce associated risks. Diabetic kidney disease is initiated by diabetes-related disturbances in glucose metabolism, which then trigger other metabolic, hemodynamic, inflammatory, and fibrotic processes that contribute to disease progression. This review summarizes existing evidence on the molecular drivers of diabetic kidney disease onset and progression, focusing on inflammatory and fibrotic mediators-factors that are largely unaddressed as primary treatment targets and for which there is increasing evidence supporting key roles in the pathophysiology of diabetic kidney disease. Results from recent clinical trials highlight promising new drug therapies, as well as a role for dietary strategies, in treating diabetic kidney disease.
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Canagliflozin and Renal Outcomes in Type 2 Diabetes and Nephropathy
Perkovic, V., Jardine, M. J., Neal, B., Bompoint, S., Heerspink, H. J. L., Charytan, D. M., Edwards, R., Agarwal, R., Bakris, G., Bull, S., et al. (2019) · New England Journal of Medicine · doi:10.1056/nejmoa1811744 · Cited by 6,189
Self-citationDapagliflozin in Patients with Chronic Kidney Disease
Heerspink, H. J. L., Stefánsson, B. V., Correa-Rotter, R., Chertow, G. M., Greene, T., Hou, F.-F., Mann, J. F. E., McMurray, J. J. V., Lindberg, M., Rossing, P., et al. (2020) · New England Journal of Medicine · doi:10.1056/nejmoa2024816 · Cited by 5,618
Once-Weekly Semaglutide in Adults with Overweight or Obesity
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Effect of finerenone on chronic kidney disease outcomes in type 2 diabetes
Bakris, G. L., Agarwal, R., Anker, S. D., Pitt, B., Ruilope, L. M., Rossing, P., Kolkhof, P., Nowack, C., Schloemer, P., Joseph, A., et al. (2020) · New England Journal of Medicine · doi:10.1056/nejmoa2025845 · Cited by 2,935
Self-citationDiabetic Kidney Disease: Challenges, Progress, and Possibilities
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Self-citationA small-molecule inhibitor of the NLRP3 inflammasome for the treatment of inflammatory diseases
Coll, R. C., Robertson, A. A. B., Chae, J. J., Higgins, S. C., Muñoz-Planillo, R., Inserra, M. C., Vetter, I., Dungan, L. S., Monks, B. G., Stutz, A., et al. (2015) · Nature Medicine · doi:10.1038/nm.3806 · Cited by 2,849
The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome-mediated inflammatory disease
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Tirzepatide versus Semaglutide Once Weekly in Patients with Type 2 Diabetes
Frías, J. P., Davies, M. J., Rosenstock, J., Pérez Manghi, F. C., Fernández Landó, L., Bergman, B. K., Liu, B., Cui, X., & Brown, K. (2021) · New England Journal of Medicine · doi:10.1056/nejmoa2107519 · Cited by 2,096
Cardiovascular events with finerenone in kidney disease and type 2 diabetes
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Self-citation
Cited by
Ndumele, C. E., Neeland, I. J., Tuttle, K. R., Chow, S. L., Mathew, R. O., Khan, S. S., Coresh, J., Baker-Smith, C. M., Carnethon, M. R., Després, J.-P., et al. (2023) · Circulation · doi:10.1161/cir.0000000000001186 · Cited by 1,405
Self-citationMann, J. F. E., Rossing, P., Bakris, G., Belmar, N., Bosch-Traberg, H., Busch, R., Charytan, D. M., Hadjadj, S., Gillard, P., Górriz, J. L., et al. (2024) · Nature Medicine · doi:10.1038/s41591-024-03133-0 · Cited by 200
“Since the molecular mechanisms of action of both drug classes on the CV system and the kidney may be complementary and largely independent of glucose lowering 6 , it has been speculated that the combination might further improve clinical outcomes.”
BackgroundSelf-citationJha, R., Lopez-Trevino, S., Kankanamalage, H. R., & Jha, J. C. (2024) · Biomedicines · doi:10.3390/biomedicines12051098 · Cited by 144
Sattar, N., Presslie, C., Rutter, M. K., & McGuire, D. K. (2024) · Diabetes Care · doi:10.2337/dci23-0041 · Cited by 70
Okello Candiya Bongomin, G. (2024) · doi:10.1016/j.heliyon.2024.e35234 · Cited by 13
Metadata
- Authors
- Tuttle, K. R., Agarwal, R., Alpers, C. E., Bakris, G. L., Brosius, F. C., Kolkhof, P., & Uribarri, J.
- Venue
- Kidney International
- Publisher
- Elsevier BV
- Published
- 2022-08
- Volume
- 102
- Issue
- 2
- Pages
- 248-260
- ISSN
- 0085-2538 (ISSN-L)
- OpenAlex
- W4281918786
- Cited by
- 668
- References
- 142
- FWCI
- 64.82
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Tuttle, K. R., Agarwal, R., Alpers, C. E., Bakris, G. L., Brosius, F. C., Kolkhof, P., & Uribarri, J. (2022). Molecular mechanisms and therapeutic targets for diabetic kidney disease. Kidney International. https://doi.org/10.1016/j.kint.2022.05.012
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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.