Ischaemic heart disease, which often manifests clinically as myocardial infarction (MI), remains a major cause of mortality worldwide. Despite the development of effective pre-clinical cardioprotective therapies, clinical translation has been disappointing. Nevertheless, the ‘reperfusion injury salvage kinase’ (RISK) pathway appears to be a promising target for cardioprotection. This pathway is crucial for the induction of cardioprotection by numerous pharmacological and non-pharmacological interventions, such as ischaemic conditioning. An important component of the cardioprotective effects of the RISK pathway involves the prevention of mitochondrial permeability transition pore (MPTP) opening and subsequent cardiac cell death. Here, we will review the historical perspective of the RISK pathway and focus on its interaction with mitochondria in the setting of cardioprotection.

缺血性心脏病在临床上通常表现为心肌梗塞（MI），仍然是全世界死亡的主要原因。尽管开发了有效的临床前心脏保护疗法，但临床转化却令人失望。尽管如此，“再灌注损伤挽救激酶”（RISK）途径似乎是心脏保护的一个有希望的目标。该途径对于通过多种药物和非药物干预措施（例如缺血调理）诱导心脏保护至关重要。RISK 通路心脏保护作用的一个重要组成部分涉及防止线粒体通透性转换孔 (MPTP) 打开和随后的心肌细胞死亡。在这里，我们将回顾 RISK 通路的历史观点，并重点关注其在心脏保护背景下与线粒体的相互作用。