Ischemia–reperfusion injury (IRI) is one of the biggest challenges for cardiovascular researchers given the huge death toll caused by myocardial ischemic disease. Cardioprotective conditioning strategies, namely pre- and post-conditioning maneuvers, represent the most important strategies for stimulating pro-survival pathways essential to preserve cardiac health. Conditioning maneuvers have proved to be fundamental for the knowledge of the molecular basis of both IRI and cardioprotection. Among this evidence, the importance of signal transducer and activator of transcription 3 (STAT3) emerged. STAT3 is not only a transcription factor but also exhibits non-genomic pro-survival functions preserving mitochondrial function from IRI. Indeed, STAT3 is emerging as an influencer of mitochondrial function to explain the cardioprotection phenomena. Studying cardioprotection, STAT3 proved to be crucial as an element of the survivor activating factor enhancement (SAFE) pathway, which converges on mitochondria and influences their function by cross-talking with other cardioprotective pathways. Clearly there are still some functional properties of STAT3 to be discovered. Therefore, in this review, we highlight the evidence that places STAT3 as a promoter of the metabolic network. In particular, we focus on the possible interactions of STAT3 with processes aimed at maintaining mitochondrial functions, including the regulation of the electron transport chain, the production of reactive oxygen species, the homeostasis of Ca²⁺ and the inhibition of opening of mitochondrial permeability transition pore. Then we consider the role of STAT3 and the parallels between STA3/STAT5 in cardioprotection by conditioning, giving emphasis to the human heart and confounders.

鉴于心肌缺血性疾病造成的巨大死亡人数，缺血再灌注损伤 (IRI) 是心血管研究人员面临的最大挑战之一。心脏保护调节策略，即预处理和后调节操作，代表了刺激维持心脏健康所必需的促生存途径的最重要策略。调节动作已被证明是了解 IRI 和心脏保护的分子基础的基础。在这些证据中，出现了信号转导和转录激活因子 3 (STAT3) 的重要性。STAT3 不仅是一种转录因子，而且还表现出非基因组促生存功能，可保护 IRI 的线粒体功能。事实上，STAT3 正在成为解释心脏保护现象的线粒体功能的影响因素。在研究心脏保护作用时，STAT3 被证明作为幸存者激活因子增强 (SAFE) 通路的一个元素至关重要，它会聚在线粒体上并通过与其他心脏保护通路的交互作用影响其功能。显然，STAT3 仍有一些功能特性有待发现。因此，在这篇综述中，我们强调了将 STAT3 作为代谢网络启动子的证据。特别是，我们关注 STAT3 与旨在维持线粒体功能的过程的可能相互作用，包括电子传递链的调节、活性氧的产生、Ca 的稳态 它聚集在线粒体上，并通过与其他心脏保护途径的相互作用来影响它们的功能。显然，STAT3 仍有一些功能特性有待发现。因此，在这篇综述中，我们强调了将 STAT3 作为代谢网络启动子的证据。特别是，我们关注 STAT3 与旨在维持线粒体功能的过程的可能相互作用，包括电子传递链的调节、活性氧的产生、Ca 的稳态 它聚集在线粒体上，并通过与其他心脏保护途径的相互作用来影响它们的功能。显然，STAT3 仍有一些功能特性有待发现。因此，在这篇综述中，我们强调了将 STAT3 作为代谢网络启动子的证据。特别是，我们关注 STAT3 与旨在维持线粒体功能的过程的可能相互作用，包括电子传递链的调节、活性氧的产生、Ca 的稳态²⁺和抑制线粒体通透性转换孔的开放。然后我们考虑 STAT3 的作用以及 STA3/STAT5 在通过条件反射保护心脏中的相似之处，强调人类心脏和混杂因素。