ArticleKorean circulation journal2026
Knockdown of ARID1A Protects H9c2 Cells Against Hypoxia/Reoxygenation (H/R)-Induced Injury by Targeting SOX9.
Article in Korean circulation journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Epigenetic Remodeling in Myocardial Reperfusion Injury: The Emerging Role of the ARID1A/SOX9 Axis.Korean circulation journal · 2026Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectivesHypoxia/reoxygenation (H/R) injury is a major contributor to cardiac damage. The role of AT-rich interaction domain 1A (ARID1A) in cardiomyocyte H/R injury and its underlying mechanisms remain unclear.
methodsAn H/R injury model was established using H9c2 cardiomyoblasts. Key assessments included cell viability (cell counting kit-8), apoptosis (Terminal deoxynucleotidyl transferase dUTP Nick End Labeling), DNA fragmentation, inflammatory cytokine levels (interleukin [IL]-1β, IL-6, IL-18), cardiac injury markers (creatine kinase-MB [CK-MB], cardiac troponin-I [cTn-I]), oxidative stress markers (lactate dehydrogenase [LDH] release, reactive oxygen species [ROS], glutathione peroxidase [GSH-Px], superoxide dismutase [SOD] activity), pyroptosis marker expression (NLR family pyrin domain containing 3 [NLRP3], caspase-1, gasdermin D [GSDMD]; Western blot), and ARID1A-SOX9 interaction (co-immunoprecipitation).
resultsH/R significantly upregulated ARID1A and SOX9 expression in H9c2 cells. ARID1A knockdown effectively attenuated H/R-induced damage, including improved cell viability, reduced apoptosis and DNA fragmentation, suppressed pro-inflammatory cytokine release (IL-1β, IL-6, IL-18), lowered CK-MB and cTn-I levels, decreased LDH release and ROS generation, enhanced antioxidant enzyme activity (GSH-Px, SOD), and reduced expression of pyroptosis markers (NLRP3, caspase-1, GSDMD). Mechanistically, ARID1A physically bound to SOX9 and promoted its expression. Crucially, the protective effects of si-ARID1A against H/R injury (apoptosis, inflammation, oxidative stress, pyroptosis) were consistently reversed by SOX9 overexpression.
conclusionsARID1A is upregulated during H/R injury and exacerbates cardiomyocyte damage by promoting apoptosis, inflammation, oxidative stress, and pyroptosis. ARID1A exerts its effects by binding to and positively regulating the expression of SOX9. Targeting the ARID1A/SOX9 axis represents a potential therapeutic strategy for mitigating H/R-induced cardiac injury.
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