About this Research Topic
Mitochondria plays its roles not only as an energy factory to power cell activities, but also being considered as the essential hub of cell activities. They are involved in many cellular physiologic activities, such as cell differentiation, cell development, cell message communication and so on. Accumulating evidence suggests that the abnormal of mitochondria, including its quality, function, anergy producing, morphology, structure or numbers in cell, are all highly related to the presence of cell aging. Most importantly for cardiovascular system, the tissue with high energy requirements, are extremely suspected to aging-related mitochondrial dysfunction. Thus, a healthy mitochondrial maintenance network is essential for cardiovascular function and adaptation to pathological stress.
The purpose of this research topic is to discuss the relationship between mitochondrial maintenance and cardiovascular aging and the potential interferences by improving cellular mitochondrial quality to relieve cardiovascular aging.
This Research Topic welcomes a range of article types that include but not limited to the following topics:
- The potential role of impaired mitochondrial biogenesis in the progression of cardiovascular aging, which may include the mitochondrial protein’s production, processing and import.
- The contribution of mitochondria quality control abnormality to cardiovascular aging, involving dysfunction in ubiquitin-proteasome system and unfolded protein response of the mitochondria, mitochondria-to- nucleus stress response, and mitochondrial DNA damage and repair.
- The underlying effects and mechanisms of mitophagy disorder and mitochondrial fusion and fission imbalance on cardiovascular aging.
- The possible biology function of mitochondrial translocation including the extracellular mitochondria and mitochondrial-derived cargo in cardiovascular aging, a process which can present as extracellular immune clearance, circulating or transferring into other cells and tissues.
- The underlying contribution of changes in mitochondrial membrane structure to cardiovascular aging.
- The regulatory roles of metabolites from mitochondrial on cardiovascular aging.
- Potential intervention strategies targeting at mitochondria to improve cardiovascular aging.
- The possible function and mechanisms of calorie restriction and circadian rhythm on mitochondrial dysfunction derived cardiovascular aging.
The purpose of this research topic is to discuss the relationship between mitochondrial maintenance and cardiovascular aging and the potential interferences by improving cellular mitochondrial quality to relieve cardiovascular aging.
This Research Topic welcomes a range of article types that include but not limited to the following topics:
- The potential role of impaired mitochondrial biogenesis in the progression of cardiovascular aging, which may include the mitochondrial protein’s production, processing and import.
- The contribution of mitochondria quality control abnormality to cardiovascular aging, involving dysfunction in ubiquitin-proteasome system and unfolded protein response of the mitochondria, mitochondria-to- nucleus stress response, and mitochondrial DNA damage and repair.
- The underlying effects and mechanisms of mitophagy disorder and mitochondrial fusion and fission imbalance on cardiovascular aging.
- The possible biology function of mitochondrial translocation including the extracellular mitochondria and mitochondrial-derived cargo in cardiovascular aging, a process which can present as extracellular immune clearance, circulating or transferring into other cells and tissues.
- The underlying contribution of changes in mitochondrial membrane structure to cardiovascular aging.
- The regulatory roles of metabolites from mitochondrial on cardiovascular aging.
- Potential intervention strategies targeting at mitochondria to improve cardiovascular aging.
- The possible function and mechanisms of calorie restriction and circadian rhythm on mitochondrial dysfunction derived cardiovascular aging.
Keywords: cardiovascular aging, mitochondria dysfunction, mechanisms, pathogenesis
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
