ReviewGlycoconjugate journal2021
Organelle stress and glycation in kidney disease.
Review in Glycoconjugate journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 8 citations in OpenAlex.
- O-Glycosylation of E-Cadherin Induced by Endoplasmic Reticulum Stress Negatively Regulates Cell Polarity and Proliferation in Acute Kidney Injury.Journal of biochemical and molecular toxicology · 2026Article
- Review
- Molecular pathways and emerging therapeutic targets in the pathogenesis of diabetic kidney disease.Frontiers in physiology · 2026Review
- Key post-translational modifications of crystallin: from mechanism to target exploration for cataract diagnosis and treatment.Molecular biology reports · 2025Review
- Oxidative-Inflammatory Crosstalk and Multi-Target Natural Agents: Decoding Diabetic Vascular Complications.Current issues in molecular biology · 2025Review
- Oleanolic acid and its analogues: promising therapeutics for kidney disease.Chinese medicine · 2024Review
- The UDPase ENTPD5 regulates ER stress-associated renal injury by mediating protein N-glycosylation.Cell death & disease · 2023Article
- Functioning and mechanisms of PTMs in renal diseases.Frontiers in pharmacology · 2023Review
- Stratification of diabetic kidney diseasesFrontiers in endocrinology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glycation of proteins is a non-enzymatic posttranslational modification. Such random modification often deranges the structure and function of a wide range of proteins, and in turn leads to cellular dysfunction and organ damage. Protein glycation is thus an important topic in understanding the molecular mechanisms of the development or progression of various kinds of diabetes-related diseases. Meanwhile, organelle stress, such as mitochondrial or endoplasmic reticulum (ER) damage, is a causal factor for cellular dysfunction. Under pathogenic conditions, mitochondrial stress and ER stress are induced by glycated proteins. Intensive research has revealed the molecular mechanism of how glycation contributes to cell fate via organelle stress. This article will summarize the most recent evidence on organelle stress and glycation in kidney disease, especially diabetic kidney disease (DKD) associated with high glycation status.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.