ArticleRespiratory research2026
Runx2 acetylation enhances pulmonary inflammation in chronic obstructive pulmonary disease through activating CDK8.
Article in Respiratory research, 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.
- Total Astragalus Saponins Modulate Ferroptosis Pathways in Cigarette Smoke and LPS-Induced Models of COPD: An in vitro and in vivo Investigation.Journal of inflammation research · 2026Article
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15 authors.
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Abstract
backgroundRunt-related transcription factor 2 (Runx2), a transcription factor of the RUNX family, is involved in various inflammatory diseases. However, the role of Runx2 was unclear in chronic obstructive pulmonary disease (COPD).
methodsPulmonary Runx2 level was compared in COPD patients and control subjects via a case-control study. Runx2 expression was detected in lung tissues of COPD mice and human bronchial epithelial (BEAS-2B) cells simulated with cigarette smoke extracts (CSE).
resultsPulmonary Runx2 expression was upregulated, and inversely associated with pulmonary function and positively correlated with inflammatory cytokines in COPD patients. Mechanistically, Runx2 activation facilitated the transcription of CDK8, a co-regulator of nuclear factor-κB (NF-κB), and inflammatory cytokines production. Luciferase report gene assay confirmed that CDK8 was the downstream target gene of Runx2. Further analysis found that CSE inhibited Runx2 ubiquitination and proteasomal degradation. Besides, CSE elevated nicotinamide adenine dinucleotide (NAD
conclusionsThese results indicated that Sirt3 depletion-induced Runx2 acetylation contributes to CDK8 activation and pulmonary inflammation in the progression of COPD.
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