ArticleAmerican journal of translational research2026
Ganoderic acid A attenuates streptozotocin-induced diabetic kidney injury: associations with mitochondrial oxidative stress and TGF-β/Smad signaling.
Article in American journal of translational research, 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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Abstract
backgroundDiabetic kidney disease (DKD) involves renal tubular epithelial injury, mitochondrial oxidative stress, and progressive fibrosis. Ganoderic acid A (GAA) has antioxidant and anti-inflammatory activities, but its potential renoprotective effects have not been fully explored in the context of DKD. This study investigated whether GAA affects high glucose (HG)-induced tubular epithelial injury
methodsHK-2 cells were pretreated with GAA before HG exposure. Cell viability, LDH release, apoptosis, oxidative stress, mitochondrial superoxide, membrane potential, ATP levels, mtDNA copy number, complex I activity, and MitoTracker Red CMXRos fluorescence were assessed. Fibrotic responses and TGF-β/Smad signaling were examined by immunoblotting and immunofluorescence, and TGF-β1 overexpression was used for mechanistic validation. Mice with STZ-DKI received GAA for 8 weeks, followed by assessments of renal function, histopathology, tubular injury, and protein expression.
resultsGAA improved HK-2 cell viability and reduced LDH release and apoptosis under HG conditions. It decreased intracellular and mitochondrial ROS, improved mitochondrial-associated parameters, and reduced NOX1/2 while increasing SOD1/2 and COX4 expression. GAA also suppressed EMT and fibrotic markers, including α-SMA, fibronectin, and collagen IV, together with reduced TGF-β1/Smad2/3 activation. TGF-β1 overexpression partially reversed these effects.
conclusionGAA attenuates HG-induced renal tubular epithelial injury
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