Cardiovascular disease (CVD) includes a number of conditions affecting the structure or function of the heart or blood vessels. At the cellular level, CVD affects the function of individual organelles, including mitochondria and endoplasmic reticulum (ER), and therefore may also have an impact on their contact sites. These contact sites can be identified as regions of biochemically distinct molecular composition, which are spatially restricted to the close vicinity of the interacting membrane fragments. The molecular assemblies forming such links provide a local environment, which can enhance the exchange of cargo or signals between organelles. The physical contact and association between mitochondria and ER temporally and spatially regulate the mitochondria/ER structure and function in cardiovascular systems, including mitochondrial bioenergetics, mitochondrial biogenesis, mitochondrial oxidative stress, mitochondrial dynamics, mitophagy, ER stress, ER unfolded protein response, and ER calcium balance.

In pathological states, such as cardiac ischaemia reperfusion, diabetic cardiomyopathy, sepsis-related myocardial depression, and myocardial infarction, mitochondria-ER contact may participate in cellular redox imbalance, ER stress, mitochondrial injury, oxidative stress, energy deletion, and programmed cell death. However, a direct link between the molecular composition of mitochondria-ER contact and CVD remains highly underappreciated and awaits further scientific attention. The upstream signals regulating mitochondria-ER contact during CVD have not been fully understood. Besides, the interactive mechanism between mitochondria and ER in response to myocardial damage deserves further in-depth investigation. In addition, the downstream events as a result of dysregulated mitochondria-ER contact require further clarification.

In this Special Issue, we invite investigators to contribute original research and review articles to discuss the regulatory mechanisms and pathological effects of mitochondria-ER contact in CVD, highlighting novel pharmaceutical strategies targeting mitochondria-ER contact for the clinical management of CVD.

Potential topics include but are not limited to the following:

• New insights into the mechanisms underlying dysregulated mitochondria-ER contact in the pathogenesis of CVD
• Clinically relevant information on the effects of therapies for CVD with a focus on mitochondria-ER contact
• Identification of mitochondria-ER contact-targeted molecules with therapeutic potential to manipulate cardiomyocyte viability and function in the treatment of CVD
• Recent advances in the knowledge and understanding of mitochondria-ER contact in CVD