Key result
Vialinin A attenuates doxorubicin-induced cardiotoxicity and improves cardiac function through SUCLG2-mediated mitochondrial protection.
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Why the study?
Doxorubicin-induced cardiotoxicity is a major limitation of cancer therapy linked to oxidative stress and mitochondrial injury, with a lack of effective natural-product-based mitigation strategies.
Vialinin A, a mushroom-derived compound, protects against doxorubicin-induced cardiotoxicity in preclinical models by engaging SUCLG2 and preserving mitochondrial function.
Hypothesis-generating for Vialinin A in DOX cardiotoxicity; leaves open clinical translation pending in vivo and human data.
Doxorubicin (DOX)-induced cardiotoxicity remains a major limitation of cancer therapy and is closely linked to oxidative stress and mitochondrial injury. However, effective natural-product-based strategies for mitigating this complication are still lacking. Here, we investigated the cardioprotective effects of Vialinin A (Via), a bioactive compound isolated from the edible mushroom Thelephora vialis, using cardiomyocytes, human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs), and a chronic mouse model of DOX-induced cardiotoxicity. Via attenuated DOX-induced cardiac injury, improved cardiac function, reduced reactive oxygen species accumulation, restored mitochondrial membrane potential, and improved ATP production. DARTS-based proteomic screening identified succinyl-CoA ligase GDP-forming subunit beta (SUCLG2) as a candidate Via-interacting protein. DARTS validation, CETSA, molecular docking, and molecular dynamics analyses provided convergent evidence consistent with cellular engagement of SUCLG2 by Via. Via increased the protease resistance and thermal stability of SUCLG2 and partially reversed the DOX-associated reduction in SUCLG2 expression. Functionally, SUCLG2 knockdown weakened Via-mediated mitochondrial protection and reduced the associated recovery of PI3K-AKT phosphorylation, whereas SUCLG2 overexpression partially alleviated DOX-induced mitochondrial dysfunction. Via also partially corrected DOX-associated changes in tricarboxylic acid cycle-related metabolites, consistent with improved mitochondrial metabolic homeostasis. Together, these findings identify Via as a mushroom-derived bioactive compound with cardioprotective activity against DOX-induced injury and support SUCLG2 as a Via-engaged, functionally relevant protein associated with mitochondrial protection.
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王 et al. (2026) studied Doxorubicin-induced cardiotoxicity. Vialinin A was evaluated. Vialinin A attenuated doxorubicin-induced cardiac injury and improved cardiac function via SUCLG2-associated mitochondrial protection in preclinical models.
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