Yang Yang ^* Ren Kaidi

• First Affiliated Hospital of Zhengzhou University, Zhengzhou, China

apoptosis by activating autophagy, ultimately protecting the heart from post-MI damage. In addition, Pengjie et al. applied advanced fetal heart quantification (Fetal HQ) to examine the impact of gestational diabetes mellitus (GDM) on fetal heart function and reported that GDM is associated with impaired right ventricular function, particularly in the later stages of pregnancy, which opens new possibilities for early heart disease prediction. Yuhu et al. took a deeper look at mitochondrial quality control by exploring the role of FUNDC1-mediated mitophagy in cardioprotection, explaining how it prevents the accumulation of damaged mitochondria and excessive mitophagy, which could lead to cell death. Finally, Shu-Ang et al. reviewed the application of pH-sensitive fluorescent proteins in cellular imaging, especially for monitoring mitochondrial pH changes, which can reveal the relationship between mitochondrial dysfunction and heart disease progression.These studies collectively increase our understanding of the intricate ways in which mitochondrial dysfunction drives the progression of heart diseases. These findings highlight the potential of mitochondrion-targeted therapies, ranging from metabolic regulation and autophagy modulation to cutting-edge imaging techniques, to reshape the future of heart disease diagnostics and treatment strategies. By investigating diverse therapeutic approaches, such as ketone-based therapies, autophagy activation, and mitophagy regulation, these studies propose new therapeutic avenues that could significantly improve clinical outcomes. Furthermore, the integration of advanced imaging technologies, such as pH-sensitive fluorescent proteins, opens up exciting possibilities for real-time monitoring of mitochondrial function, providing deeper insights into disease mechanisms and treatment efficacy. Together, these articles not only refine our knowledge of the role of mitochondria in cardiovascular diseases but also set the stage for novel therapeutic innovations that could have a lasting impact on heart disease management and prevention.As research has revealed the diverse roles of mitochondrial dysfunction in heart diseases such as heart failure, myocardial infarction, and ischemic conditions, the potential of mitochondria-targeting therapies to revolutionize clinical practice has become increasingly clear. These therapies, including metabolic modulation, autophagy enhancement, and advanced imaging techniques, could offer significant advantages by addressing the underlying causes of disease rather than just alleviating symptoms. For example, ketone-based therapies have shown promise in heart failure treatment by improving mitochondrial function, reducing oxidative stress, and enhancing cellular energy production, which may stabilize cardiac function and reduce the burden on a failing heart [5]. Similarly, autophagy activation, as demonstrated in studies on Sterofundin, could mitigate myocardial infarction damage by promoting mitochondrial turnover and reducing oxidative stress, thus improving recovery outcomes and preventing long-term complications such as heart failure [6]. Additionally, advanced imaging techniques such as pH-sensitive fluorescent proteins could enable real-time monitoring of mitochondrial function, providing insights into disease progression and helping tailor personalized treatment strategies [7]. However, challenges remain, particularly in the development of safe and effective drug delivery systems to target mitochondria precisely. Advancements in nanoparticle-based delivery methods will be key to improving precision and safety, while the variability in patient responses calls for personalized treatment strategies. The development of biomarkers to predict patient responses will be essential for optimizing therapeutic outcomes, ensuring that the most effective treatments are delivered.