ArticleAmerican journal of translational research2022
Inhibition of histone methyltransferase G9a effectively protected the kidney against ischemia-reperfusion injury.
Article in American journal of translational research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 3 citations in OpenAlex.
- Exacerbation of renal interstitial fibrosis by the UHRF1/G9a axis through epigenetic silencing of KLF15.Renal failure · 2026Article
- Histone methylation of kidney disease: fact or fantasy?Renal failure · 2025Review
- Astragaloside IV relieves passive heymann nephritis and podocyte injury by suppressing the TRAF6/NF-κb axis.Renal failure · 2024Article
- Loss of renal tubular G9a benefits acute kidney injury by lowering focal lipid accumulation via CES1.EMBO reports · 2023Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study examined whether BIX01294, a histone methyltransferase G9a inhibitor, effectively preserves the renal function following acute kidney ischemia-reperfusion (AKIR) injury. Adult-male-SD rats (n = 24) were equally categorized into Group 1 (sham-operated control), Group 2 (AKIR + 1.0 cc N/S I.P. injection), and Group 3 (AKIR + BIX01294/5 mg/Kg by I.P. administration at 3 h after the procedure) and the kidneys were harvested at day-3 post-IR procedure. The results showed that by day 3, the levels of creatinine and the blood urea nitrogen (BUN) were significantly higher in group 3 and more significantly higher in group 2 than in group 1 (all P < 0.0001). The protein expression of upstream (TLR-2/TLR-4/MyD88/TRAF6/p-NF-κB) and downstream (IL-1ß/IL-6/TNF-α) inflammatory signaling molecules exhibited a pattern identical to that of creatinine levels among the groups (all P < 0.0001). The protein expression of oxidative stress (NOX-1/NOX-2), MAP kinase family members (ASK1/MKK4/MKK7/JNK/p-38/p-ERK1/2), apoptosis (cleaved-caspase3/cleaved-caspase8/cleaved-PARP/mitochondrial-Bax), fibrosis (Smad3/TGF-ß), and mitochondrial-damaged markers (cyclophilin D/cytosolic-cytochrome-C) displayed a pattern identical to that of creatinine levels among the groups (all P < 0.0001). The kidney injury score, fibrosis, cellular expression of inflammation (CD68+cells), and glomerulus/renal-tubular damaged markers (Snail/KIM-1/WT-1) exhibited an identical pattern, whereas the cellular expression of podocyte component (synaptopodin) displayed an opposite pattern of creatinine levels among the groups (all P < 0.0001). Therefore, the G9a inhibitor effectively protected kidneys against IR injury.
Indexed as
Identifiers
35836849PMC9274564W4285612560What Socratic holds
Registered trials
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