ArticleInternational journal of general medicine2025
Compound Tinglizi Decoction-Containing Serum Is Associated with Inhibition of PANoptosis in Cardiomyocytes via SIRT3-Related Chaperone-Mediated Autophagy of AIM2.
Article in International journal of general medicine, 2025. 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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Who cites it
1 citing paper in PubMed.
- Astragaloside IV mitigated cadmium-induced glandular gastric injury in ducks by inhibiting PANoptosis.Frontiers in veterinary science · 2026Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Septic cardiomyopathy (SCM) is a life-threatening complication of sepsis with no specific therapeutic options. Recent evidence suggests that PANoptosis, a programmed cell death pathway, contributes to myocardial injury in sepsis. Compound Tinglizi Decoction (CTLZC), a traditional Chinese herbal formula, has shown potential cardioprotective effects, yet the underlying biochemical mechanisms remain unclear. Methods: A rat model of SCM was established to investigate the effect of CTLZC-containing serum on myocardial injury. Primary cardiomyocytes were treated with CTLZC-containing serum, and SIRT3 expression was modulated via overexpression and knockdown plasmids. Cell viability, PANoptosis markers, and chaperone-mediated autophagy (CMA) proteins were assessed through CCK-8, TUNEL staining, RT-qPCR, Western blotting, ELISA, and Co-IP assays. Results: CTLZC-containing serum enhanced cardiomyocyte viability and significantly upregulated SIRT3 expression. It inhibited the expression of PANoptosis-related molecules (AIM2, ZBP1, RIPK1, RIPK3, FADD, and caspase-8) and promoted the expression of CMA-related proteins HSC70 and LAMP2A. SIRT3 knockdown reversed these effects and increased the release of biochemical markers of myocardial injury (LDH, CK-MB) and inflammatory cytokines (TNF-α, IL-1β, IL-18). Co-IP confirmed that AIM2 interacts with HSC70, indicating lysosomal degradation via CMA. Conclusion: CTLZC-containing serum attenuates inflammatory and cell death responses in septic cardiomyopathy, likely through a SIRT3-associated modulation of chaperone-mediated autophagy and PANoptosis. These findings highlight the biochemical regulatory role of SIRT3 in mediating autophagic and inflammatory pathways during SCM, offering new insights into potential therapeutic targets.
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