ReviewClinical and experimental nephrology2014
A possible structural basis behind the pathogenic role of apolipoprotein E hereditary mutations associated with lipoprotein glomerulopathy.
Review in Clinical and experimental nephrology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Lipoprotein(a) and the risk of type I cardiorenal syndrome in patients with coronary artery disease: A retrospective clinical study.International journal of cardiology. Heart & vasculature · 2025Article
- Thermodynamic destabilization and aggregation propensity as the mechanism behind the association of apoE3 mutants and lipoprotein glomerulopathy.Journal of lipid research · 2018Article
- Apolipoprotein E - A Multifunctional Protein with Implications in Various Pathologies as a Result of Its Structural Features.Computational and structural biotechnology journal · 2017Review
- Pathogenesis, histopathologic findings and treatment modalities of lipoprotein glomerulopathy: A review.Jornal brasileiro de nefrologiaReview
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Single amino acid mutations in apolipoprotein E (apoE) have been associated with the development of the rare kidney disease lipoprotein glomerulopathy (LPG). Although the genetic linkage to disease development is well established, the mechanism of pathogenesis is largely unknown, limiting therapeutic insight. Here, we summarize current knowledge in the field and focus on the possible effects of LPG-associated mutations on the structure of apoE. Recent findings have suggested that mutation-induced folding perturbations in apoE lead to structural destabilization and aggregation, effects that may underlie lipoprotein thrombi accumulation in the glomerulus, a hallmark of LPG. The recognition that structural destabilization may underlie the association between apoE mutations and LPG can be key for development of new innovative treatments for this rare disease.
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