ReviewBiology2026
Fatty Kidney Disease: From Renal Lipid Dysregulation to Fibrosis.
Review in Biology, 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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Authors and funding
4 authors.
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Abstract
Progression to fibrosis is a major complication of chronic kidney disease (CKD) in obesity, type 2 diabetes, hypertension, and metabolic syndrome, yet effective antifibrotic therapies remain limited. Here, we review how disordered renal energy metabolism-ectopic lipid accumulation, impaired fatty acid oxidation (FAO), and a compensatory shift toward glycolysis-drives tubulointerstitial fibrosis in fatty kidney disease. Lipid overload in tubular, glomerular, and vascular cells arises from increased uptake via scavenger and lipoprotein receptors, enhanced lipogenesis, and reduced lipid catabolism and clearance. Spatial lipidomic studies further reveal nephron-segment-specific lipid signatures and obesity-associated oxidized phospholipids linked to glomerular inflammation. Lipotoxicity, mitochondrial damage, and associated innate-immune signaling, ferroptosis, cellular senescence, and adipose-derived mediators (including leptin, adiponectin, and a locally active renin-angiotensin system) converge on myofibroblast activation from pericytes, fibroblasts, and other resident cells. We discuss established and emerging therapies targeting this metabolic axis-peroxisome proliferator-activated receptor-α (PPARα) modulators, sodium-glucose cotransporter-2 (SGLT2) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists, and the mineralocorticoid receptor antagonist finerenone-and propose that restoring metabolic flexibility, by rescuing FAO while limiting maladaptive glycolysis, offers a promising disease-modifying strategy for fatty kidney disease.
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