Vascular remodelling, the adaptive response to various physiological and pathophysiological alterations, is the pathological basis for several vascular diseases. The pathological vascular remodelling may buffer (expansive) or aggravate (constrictive) lumen encroachment caused by increases in vessel wall due to atherosclerosis, hypertension, aneurysm, etc. In addition, vascular remodelling may also contribute to target organ damage, via interfering with the blood supply to major body organs such as heart, brain and kidney. Understanding the underlying mechanism of the regulation of vascular remodelling may be helpful for discovering potential therapeutic targets and strategies. Both inside-out and outside-in hypothesis have been put forward to describe mechanisms of vascular remodelling. However, the molecular mechanisms responsible for adventitial fibroblast activation (adventitial layer), smooth muscle cell phenotypic switch (media layer), endothelial cell dysfunction (lumen layer), and their interactions are still elusive. Recent studies indicate that metabolic or mitochondrial reprogramming plays critical roles in these cell events. Therefore, strategies focusing on mitochondrial dysfunction and metabolism reprograming may be promising in the future.
Cardiovascular disease (CVD) is one of the dominant causes of death in several countries. In recent years, vascular remodelling has been one of the focuses of molecular biology research on arterial vascular related diseases represented by hypertension. During vascular remodelling, cells undergo changes in proliferation, migration, apoptosis, differentiation, as well as changes in their extracellular matrix (ECM). Mitochondrial dysfunction and metabolism reprograming are closely associated with several types of cells activation during vascular remodelling and related target organ damage.
In this Research Topic, we would like to create a forum for current advances on cellular and physiological mechanisms, especially for mitochondrial dysfunction and metabolism reprograming, linking vascular remodelling as well as pathophysiological and clinical consequences of related target organ damage, which may afford promising strategies for CVD related to vascular remodelling.
We welcome papers in the following topics but not limited to:
1) The role of abnormal mitochondrial morphology, motility and function in vascular remodelling, including related target organ damage, and underlying cellular and molecular mechanisms.
2) The role of noncoding RNA in vascular remodelling and related diseases and underlying mechanisms.
3) Translational study on mitochondria related therapy for vascular remodelling and related diseases in large animal models.
4) The mitochondrial and metabolic control of phenotypic switch of adventitial fibroblasts and vascular smooth cells.
5) Integrative medicine using evidence-based medicine and bioinformatics approaches to study vascular remodelling and related diseases.
6) The mechanisms of anti-cancer treatments induced cardiovascular injury.
Vascular remodelling, the adaptive response to various physiological and pathophysiological alterations, is the pathological basis for several vascular diseases. The pathological vascular remodelling may buffer (expansive) or aggravate (constrictive) lumen encroachment caused by increases in vessel wall due to atherosclerosis, hypertension, aneurysm, etc. In addition, vascular remodelling may also contribute to target organ damage, via interfering with the blood supply to major body organs such as heart, brain and kidney. Understanding the underlying mechanism of the regulation of vascular remodelling may be helpful for discovering potential therapeutic targets and strategies. Both inside-out and outside-in hypothesis have been put forward to describe mechanisms of vascular remodelling. However, the molecular mechanisms responsible for adventitial fibroblast activation (adventitial layer), smooth muscle cell phenotypic switch (media layer), endothelial cell dysfunction (lumen layer), and their interactions are still elusive. Recent studies indicate that metabolic or mitochondrial reprogramming plays critical roles in these cell events. Therefore, strategies focusing on mitochondrial dysfunction and metabolism reprograming may be promising in the future.
Cardiovascular disease (CVD) is one of the dominant causes of death in several countries. In recent years, vascular remodelling has been one of the focuses of molecular biology research on arterial vascular related diseases represented by hypertension. During vascular remodelling, cells undergo changes in proliferation, migration, apoptosis, differentiation, as well as changes in their extracellular matrix (ECM). Mitochondrial dysfunction and metabolism reprograming are closely associated with several types of cells activation during vascular remodelling and related target organ damage.
In this Research Topic, we would like to create a forum for current advances on cellular and physiological mechanisms, especially for mitochondrial dysfunction and metabolism reprograming, linking vascular remodelling as well as pathophysiological and clinical consequences of related target organ damage, which may afford promising strategies for CVD related to vascular remodelling.
We welcome papers in the following topics but not limited to:
1) The role of abnormal mitochondrial morphology, motility and function in vascular remodelling, including related target organ damage, and underlying cellular and molecular mechanisms.
2) The role of noncoding RNA in vascular remodelling and related diseases and underlying mechanisms.
3) Translational study on mitochondria related therapy for vascular remodelling and related diseases in large animal models.
4) The mitochondrial and metabolic control of phenotypic switch of adventitial fibroblasts and vascular smooth cells.
5) Integrative medicine using evidence-based medicine and bioinformatics approaches to study vascular remodelling and related diseases.
6) The mechanisms of anti-cancer treatments induced cardiovascular injury.
