Tayal Rohit, Mannan Ashi, Singh Shareen, Dhiman Sonia, Singh Thakur Gurjeet
Chitkara College of Pharmacy, Chitkara University, Rajpura, Punjab, India.
Curr Cardiol Rev. 2025;21(2):42-77. doi: 10.2174/011573403X322928241021100631.
The coexistence of cancer and heart disease, both prominent causes of illness and death, is further exacerbated by the detrimental impact of chemotherapy. Anthracycline-induced cardiotoxicity is an unfortunate side effect of highly effective therapy in treating different types of cancer; it presents a significant challenge for both clinicians and patients due to the considerable risk of cardiotoxicity. Despite significant progress in understanding these mechanisms, challenges persist in identifying effective preventive and therapeutic strategies, rendering it a subject of continued research even after three decades of intensive global investigation. The molecular targets and signaling pathways explored provide insights for developing targeted therapies, emphasizing the need for continued research to bridge the gap between preclinical understanding and clinical applications. This review provides a comprehensive exploration of the intricate mechanisms underlying anthracycline-induced cardiotoxicity, elucidating the interplay of various signaling pathways leading to adverse cellular events, including cardiotoxicity and death. It highlights the extensive involvement of pathways associated with oxidative stress, inflammation, apoptosis, and cellular stress responses, offering insights into potential and unexplored targets for therapeutic intervention in mitigating anthracycline-induced cardiac complications. A comprehensive understanding of the interplay between anthracyclines and these complexes signaling pathways is crucial for developing strategies to prevent or mitigate the associated cardiotoxicity. Further research is needed to outline the specific contributions of these pathways and identify potential therapeutic targets to improve the safety and efficacy of anthracycline-based cancer treatment. Ultimately, advancements in understanding anthracycline-induced cardiotoxicity mechanisms will facilitate the development of more efficacious preventive and treatment approaches, thereby improving outcomes for cancer patients undergoing anthracycline-based chemotherapy.
癌症和心脏病都是导致疾病和死亡的主要原因，二者并存，而化疗的有害影响又进一步加剧了这种情况。蒽环类药物引起的心脏毒性是治疗不同类型癌症的高效疗法产生的不幸副作用；由于心脏毒性风险相当大，它给临床医生和患者都带来了重大挑战。尽管在理解这些机制方面取得了重大进展，但在确定有效的预防和治疗策略方面仍然存在挑战，即使经过全球三十年的深入研究，它仍然是一个持续研究的课题。所探索的分子靶点和信号通路为开发靶向治疗提供了见解，强调需要持续研究以弥合临床前理解与临床应用之间的差距。本综述全面探讨了蒽环类药物引起心脏毒性的复杂机制，阐明了导致不良细胞事件（包括心脏毒性和死亡）的各种信号通路之间的相互作用。它强调了与氧化应激、炎症、细胞凋亡和细胞应激反应相关的通路的广泛参与，为减轻蒽环类药物引起的心脏并发症的治疗干预提供了潜在的和未被探索的靶点的见解。全面了解蒽环类药物与这些复杂信号通路之间的相互作用对于制定预防或减轻相关心脏毒性的策略至关重要。需要进一步研究来概述这些通路的具体作用，并确定潜在的治疗靶点，以提高基于蒽环类药物的癌症治疗的安全性和有效性。最终，对蒽环类药物引起心脏毒性机制的理解取得进展将有助于开发更有效的预防和治疗方法，从而改善接受基于蒽环类药物化疗的癌症患者的治疗效果。
