Cited by 163Advanced Glycation End Products researchChronic Kidney Disease and DiabetesRenal Diseases and Glomerulopathies

Advanced glycation end products mediated cellular and molecular events in the pathology of diabetic nephropathy

Open access
Kumar Pasupulati, Anil, Chitra, P. Swathi, Reddy, G. Bhanuprakash·2016·Biomolecular Concepts

Abstract

Diabetic nephropathy (DN) is a major cause of morbidity and mortality in diabetic patients and a leading cause of end-stage renal disease (ESRD). Degenerative changes such as glomerular hypertrophy, hyperfiltration, widening of basement membranes, tubulointerstitial fibrosis, glomerulosclerosis and podocytopathy manifest in various degrees of proteinuria in DN. One of the key mechanisms implicated in the pathogenesis of DN is non-enzymatic glycation (NEG). NEG is the irreversible attachment of reducing sugars onto free amino groups of proteins by a series of events, which include the formation of Schiff’s base and an Amadori product to yield advanced glycation end products (AGEs). AGE modification of client proteins from the extracellular matrix induces crosslinking, which is often associated with thickening of the basement membrane. AGEs activate several intracellular signaling cascades upon interaction with receptor for AGEs (RAGE), which manifest in aberrant cellular responses such as inflammation, apoptosis and autophagy, whereas other receptors such as AGE-R1, AGE-R3 and scavenger receptors also bind to AGEs and ensue endocytosis and degradation of AGEs. Elevated levels of both serum and tissue AGEs are associated with adverse renal outcome. Increased evidence supports that attenuation of AGE formation and/or inhibition of RAGE activation manifest(s) in improving renal function. This review provides insights of NEG, discusses the cellular and molecular events triggered by AGEs, which manifest in the pathogenesis of DN including renal fibrosis, podocyte epithelial-mesenchymal transition and activation of renin-angiotensin system. Therapies designed to target AGEs, such as inhibitors of AGEs formation and crosslink breakers, are discussed.

Integrity signals

Registry

Crossref · 10.1515/bmc-2016-0021

Cites

110 of 110 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

We couldn’t retrieve this paper’s full text, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Kumar Pasupulati, A., Chitra, P. S., & Reddy, G. B.
Affiliations
  • Department of Biochemistry, University of Hyderabad, Hyderabad 500 046, India
  • National Institute of Nutrition (IN)
Corresponding author
Reddy, G. Bhanuprakash
Venue
Biomolecular Concepts
Published
2016-11-07
Volume
7
Issue
5-6
Pages
293-309
ISSN
  • 1868-5021 (ISSN-L)
  • 1868-503X
OpenAlex
W2550737605
Cited by
163
References
110
Citations by year
2026: 7 · 2025: 18 · 2024: 19 · 2023: 21 · 2022: 25 · 2021: 29 · 2020: 19 · 2019: 9 · 2018: 8 · 2017: 8
FWCI
0.86
Type
journal article
Language
en
Open access
Locations
  • BioMolecular Concepts (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
Defence Research and Development Organisation
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
  • Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
  • Health Sciences › Medicine › Nephrology › Renal Diseases and Glomerulopathies
Keywords
diabetic nephropathy, advanced glycation end products, glycation, receptor for advanced glycation end products, renal fibrosis, renin-angiotensin system, proteinuria, glomerulosclerosis, inflammation, apoptosis, autophagy
MeSH terms
Receptor for Advanced Glycation End Products, Diabetic Nephropathies, Humans, Protein Binding, Renin-Angiotensin System, Signal Transduction, Glycation End Products, Advanced, Podocytes, Epithelial-Mesenchymal Transition, Molecular Targeted Therapy

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