About this Research Topic
Mitochondria, once considered mere cellular powerhouses, are increasingly recognized as pivotal players in the intricate web of cellular functions. These double-membraned organelles play a critical role in energy production through oxidative phosphorylation and the utilization of ketone bodies. Additionally, they are involved in reactive oxygen species generation, buffering excess cytosolic calcium, and are signaling hub for numerous cellular processes, contributing to the overall metabolic balance within the cell. Mitochondria in the cell exist in a dynamic reticular network that is critical for their proper functioning. In this network, they constantly undergo dynamic and tightly regulated fission and fusion processes, necessary for quality control and to meet the energy demands of the cell.
Mitochondrial stress or disturbances in mitochondrial function may lead to the development and/or progression of endothelial dysfunction and could precede vascular diseases. Mitochondrial biogenesis is one of the potentially protective mechanisms that allow endothelial cells, subjected to moderate metabolic stress or proinflammatory stimuli, to maintain cellular energy homeostasis and prevent cell death. Interestingly, increased oxidative stress, together with the translocation of mitochondrial DNA to the cytosol, are reported as hallmarks of mitochondrial dysregulation that leads to mitophagy (mitochondria-specific autophagy of damaged mitochondria) and concomitant cell death. It should be noted that the efficient removal of defective mitochondria underlies the quality control mechanisms that support cell viability and survival of the organism. Mitochondrial location in the cell as well as their dynamic interaction within the network is also associated with the regulation of their communication with other organelles, such as the endoplasmic reticulum and the nucleus.
The role of mitochondria in cell stress response stimuli involves the activation of some adaptive mechanisms that enable the cell to survive. Recently, attention has focused on the newly discovered function of mitochondria as a signal transmission hub for both intra- and extracellular physiological events. The existence of extracellular mitochondria is postulated as an example of cell-to-cell communication mechanisms preceded by stress stimuli. However, the detailed mechanisms and regulations in endothelial cells have not been described to date.
In this Research Topic we would like to gather original research articles and review papers presenting the multifaceted role of mitochondria in the context of endothelial dysfunction and its profound implications for metabolic disorders. Emphasizing the pivotal role of mitochondria in maintaining vascular homeostasis, we would like to highlight the intricate interplay between mitochondrial dynamics, bioenergetics, and signaling pathways within endothelial cells, and to delve into mitochondrial contribution to endothelial dysfunction—a hallmark of various metabolic disorders, including diabetes and obesity, but also cancer.
The articles in this Research Topic may provide novel insights into the potential of endothelial mitochondria as a promising therapeutic target in mitigating the development and progression of cardiovascular diseases, the major cause of mortality and serious disability worldwide.
Topic Editors declare no conflict of interest.
Mitochondrial stress or disturbances in mitochondrial function may lead to the development and/or progression of endothelial dysfunction and could precede vascular diseases. Mitochondrial biogenesis is one of the potentially protective mechanisms that allow endothelial cells, subjected to moderate metabolic stress or proinflammatory stimuli, to maintain cellular energy homeostasis and prevent cell death. Interestingly, increased oxidative stress, together with the translocation of mitochondrial DNA to the cytosol, are reported as hallmarks of mitochondrial dysregulation that leads to mitophagy (mitochondria-specific autophagy of damaged mitochondria) and concomitant cell death. It should be noted that the efficient removal of defective mitochondria underlies the quality control mechanisms that support cell viability and survival of the organism. Mitochondrial location in the cell as well as their dynamic interaction within the network is also associated with the regulation of their communication with other organelles, such as the endoplasmic reticulum and the nucleus.
The role of mitochondria in cell stress response stimuli involves the activation of some adaptive mechanisms that enable the cell to survive. Recently, attention has focused on the newly discovered function of mitochondria as a signal transmission hub for both intra- and extracellular physiological events. The existence of extracellular mitochondria is postulated as an example of cell-to-cell communication mechanisms preceded by stress stimuli. However, the detailed mechanisms and regulations in endothelial cells have not been described to date.
In this Research Topic we would like to gather original research articles and review papers presenting the multifaceted role of mitochondria in the context of endothelial dysfunction and its profound implications for metabolic disorders. Emphasizing the pivotal role of mitochondria in maintaining vascular homeostasis, we would like to highlight the intricate interplay between mitochondrial dynamics, bioenergetics, and signaling pathways within endothelial cells, and to delve into mitochondrial contribution to endothelial dysfunction—a hallmark of various metabolic disorders, including diabetes and obesity, but also cancer.
The articles in this Research Topic may provide novel insights into the potential of endothelial mitochondria as a promising therapeutic target in mitigating the development and progression of cardiovascular diseases, the major cause of mortality and serious disability worldwide.
Topic Editors declare no conflict of interest.
Keywords: energy metabolism in endothelium, reactive oxygen species, endothelial dysfunction, functioning of mitochondria in metabolic disorders, endothelial mitochondria;, metabolic disorders
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