Salidroside Alleviates Mobocertinib-Induced Cardiotoxicity by Improving Cardiac Electrophysiology.
C, Y., X, L., X, Z., P, W., X, L., D, L., G, Z., M, L., X, Z., & G, L. (2026). Salidroside Alleviates Mobocertinib-Induced Cardiotoxicity by Improving Cardiac Electrophysiology.. Cardiovascular toxicology. https://doi.org/10.1007/s12012-026-10169-w
C Y, X L, X Z, P W, X L, D L, et al. Salidroside Alleviates Mobocertinib-Induced Cardiotoxicity by Improving Cardiac Electrophysiology.. Cardiovascular toxicology. 2026; doi: 10.1007/s12012-026-10169-w
C Y, X L, X Z, et al. Salidroside Alleviates Mobocertinib-Induced Cardiotoxicity by Improving Cardiac Electrophysiology.[J]. Cardiovascular toxicology. 2026. DOI: 10.1007/s12012-026-10169-w.
@article{c2026,
author = {Yan C and Liu X and Zhang X and Wei P and Li X and Li D and Zhang G and Li M and Zang X and Lu G},
title = {Salidroside Alleviates Mobocertinib-Induced Cardiotoxicity by Improving Cardiac Electrophysiology.},
journal = {Cardiovascular toxicology},
year = {2026},
doi = {10.1007/s12012-026-10169-w},
note = {PMID: 42570138},
}
TY - JOUR AU - Yan C AU - Liu X AU - Zhang X AU - Wei P AU - Li X AU - Li D AU - Zhang G AU - Li M AU - Zang X AU - Lu G TI - Salidroside Alleviates Mobocertinib-Induced Cardiotoxicity by Improving Cardiac Electrophysiology. T2 - Cardiovascular toxicology PY - 2026 DO - 10.1007/s12012-026-10169-w AN - PMID:42570138 ER -
Mobocertinib, a tyrosine kinase inhibitor approved for EGFR exon 20 insertion-mutated non-small cell lung cancer, induces cardiotoxicity manifesting as QT prolongation. Salidroside, a bioactive compound from Rhodiola rosea, exhibits cardioprotective properties. We investigated electrophysiological mechanisms underlying mobocertinib cardiotoxicity and salidroside's protective efficacy using Langendorff-perfused rat hearts and neonatal rat cardiomyocytes (NRCMs). Hearts were treated with escalating mobocertinib concentrations (214, 428, 856 nM) with or without salidroside (20 μM) pretreatment; cardiac parameters including heart rate, PR, JT, QTc intervals and conduction were mapped via high-resolution multichannel electrophysiology. NRCMs underwent chronic mobocertinib exposure with/without salidroside, followed by transcriptomic sequencing, qRT-PCR, and western blot validation. Mobocertinib concentration-dependently prolonged PR, JT, QTc intervals, increased conduction time/heterogeneity, reduced heart rate/velocity, and JT/QTc prolongation persisted after washout. Salidroside pretreatment markedly attenuated these abnormalities. In NRCMs, mobocertinib prolonged field potential duration and impaired conduction; salidroside normalized parameters. Transcriptomic analysis identified enrichment in calcium signaling, aldosterone synthesis, cGMP-PKG, and adrenergic pathways. Notably, Atp2b2 was upregulated in mobocertinib group but downregulated in salidroside combination group, whereas Agtr1b showed opposite pattern. Thus, salidroside mitigates mobocertinib-induced electrophysiological toxicity by modulating Atp2b2/Agtr1b-related signaling networks, providing a novel cardioprotective strategy against mobocertinib-associated cardiotoxicity.