ReviewInternational journal of molecular sciences2026
Molecular Mechanisms of APOL1-Associated Kidney Disease.
Review in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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3 authors.
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Abstract
The discovery of apolipoprotein L1 (APOL1) risk polymorphisms has significantly changed our knowledge of kidney disease susceptibility and development in African American populations. Several non-diabetic kidney disorders, such as focal segmental glomerulosclerosis (FSGS), collapsing glomerulopathy, HIV-associated nephropathy (HIVAN), and accelerated chronic kidney disease (CKD) development, are significantly more likely to occur in people with two coding variations, G1 and G2. The significance of context-dependent pathogenic processes is highlighted by the poor penetrance and remarkable phenotypic variety of APOL1-associated kidney disease, despite its substantial impact. This review synthesizes current knowledge of APOL1 biology through a molecular framework, emphasizing gain-of-toxic-function effects of risk variants in podocytes, dysregulated ion fluxes, mitochondrial dysfunction, impaired proteostasis, and activation of innate immune and inflammatory signaling pathways. We describe how the well-recognized "second-hit" paradigm has a biological basis, driven by strong inducibility by interferons and immunological activation, as well as strict basal regulation of APOL1 expression. Lastly, we explore future approaches to precision nephrology and highlight translational advancements, such as
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