ArticleFrontiers in pharmacology2026
Isoniazid subverting erythrocyte homeostasis: implications for tuberculosis therapy.
Article in Frontiers in pharmacology, 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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Abstract
Isoniazid (INH) is a frontline anti-tuberculosis drug. Understanding the molecular mechanisms by which INH affects antioxidant defence in human blood cells, particularly erythrocytes vulnerable to oxidative damage, remains essential to improving therapy safety. Here, the transcriptomic data of tuberculosis INH therapy-treated HepG2 cell line were analyzed to identify differentially expressed genes (DEGs). DEGs were cross-referenced with curated oxidative stress (OS) gene sets from GeneCards, and protein-protein interaction (PPI) networks were constructed to identify hub OS genes associated with INH treatment-induced OS. Biochemical assays assessed antioxidant enzyme activities (SOD, GPx, CAT and ROS), erythrocyte morphology, membrane integrity, and calcium involvement following INH exposure
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