About this Research Topic
Endothelial cells play a critical role in controlling changes in diameter along the length of the different segments of resistance arteries within the microvascular network, which involves the coordination of functions of different cell types. In addition to endothelial cells, the wall of resistance vessels is mainly constituted by smooth muscle cells and perivascular nerves (sympathetic and sensitive nerve terminals). Thus, control of vascular function depends on fine communication between various cell types that are not always in direct contact and the endothelium is in a strategic position to integrate signaling between changes in blood flow and the vasomotor activity of the vessel wall.
One important mechanism of endothelial cell signaling is mediated by the release of autocrine/paracrine signals. Nitric oxide (NO) and prostaglandins are widely recognized autocrine/paracrine signals that play diverse roles in the endothelial cell-mediated control of vascular function. Although connexin hemichannels (i.e., half of gap junction channel) and pannexin channels may contribute to the release of these signals, the coordination of endothelial cell signaling also relies on direct gap junction channel-mediated communication among cells of the vessel wall. As the homeostasis of each cell in the organism depends on the proper function of the vascular system, especially resistance arteries, it is essential to improve and advance our understanding of the mechanisms involved in the integrative regulation of vascular function by endothelial cell signaling.
This Research Topic intends to combine original research, mini-reviews, commentaries, and opinion papers related to the study and discussion of:
1) Mechanisms of autocrine/paracrine signaling in the vessel wall.
2) Pathways of endothelial cell signaling.
3) Transduction mechanisms involved in the control of endothelial cell function.
4) Control of endothelial cell function through the interaction of physical and biochemical stimuli.
5) Alterations in endothelial cell signaling associated with the progression of cardiovascular-related diseases.
Topic Editor Prof. Daniel González is the holder of the patent WO2009/059271 A1, related to the Diagnosis and Treatment of Cardiac Disorders. Prof. Xavier Figuero declares no conflicts of interest with regards to the Research Topic .
One important mechanism of endothelial cell signaling is mediated by the release of autocrine/paracrine signals. Nitric oxide (NO) and prostaglandins are widely recognized autocrine/paracrine signals that play diverse roles in the endothelial cell-mediated control of vascular function. Although connexin hemichannels (i.e., half of gap junction channel) and pannexin channels may contribute to the release of these signals, the coordination of endothelial cell signaling also relies on direct gap junction channel-mediated communication among cells of the vessel wall. As the homeostasis of each cell in the organism depends on the proper function of the vascular system, especially resistance arteries, it is essential to improve and advance our understanding of the mechanisms involved in the integrative regulation of vascular function by endothelial cell signaling.
This Research Topic intends to combine original research, mini-reviews, commentaries, and opinion papers related to the study and discussion of:
1) Mechanisms of autocrine/paracrine signaling in the vessel wall.
2) Pathways of endothelial cell signaling.
3) Transduction mechanisms involved in the control of endothelial cell function.
4) Control of endothelial cell function through the interaction of physical and biochemical stimuli.
5) Alterations in endothelial cell signaling associated with the progression of cardiovascular-related diseases.
Topic Editor Prof. Daniel González is the holder of the patent WO2009/059271 A1, related to the Diagnosis and Treatment of Cardiac Disorders. Prof. Xavier Figuero declares no conflicts of interest with regards to the Research Topic .
Keywords: endothelial, signaling, resistance arteries, physiology
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