Thoracic aortic aneurysms and dissections (TAAD) are a life-threatening disease that accounts for a significant proportion of aortic-related deaths. Although hypertension and the presence of a congenital bicuspid aortic valve (BAV) are risk factors for the disease, a genetic predisposition also plays a prominent role in the etiology. Despite its sudden and unpredictable nature, recent advancements in understanding the mechanisms of TAAD have reported that hemodynamic disturbance, inflammatory factors, and metabolic stress contribute greatly to aortic wall modeling. However, effective measures to prevent its onset or progression are currently unavailable.
Therefore, there is a critical need to develop new treatment strategies for TAAD. However, a major barrier to this goal is a poor understanding of the molecular mechanisms that trigger and promote aortic degeneration in sporadic TAAD. The histopathological hallmark of TAAD is aortic medial degeneration, characterized by proteoglycan accumulation (pooling), elastic fiber fragmentation and smooth muscle cell degeneration. This process contributes to vascular remodeling and weakening of the aortic wall, resulting in aortic aneurysm, dissection, and rupture.
This Research Topic aims to address this important unmet clinical need by elucidating the most recent cellular and molecular pathophysiologic mechanisms governing TAAD development, which may lead to pharmaceutical approaches for preventing TAAD progression. The long-term goal of this Research Topic is to improve our understanding of the physiology and pathobiology of aortic wall degeneration and remolding to develop new pharmacological strategies to prevent TAAD formation and progression. This Research Topic will cover the common subtypes of TAAD, including Marfan syndrome, vascular Ehlers-Danlos, Loeys-Dietz, and familial and unifamilial thoracic aortic aneurysm and dissection.
To achieve this goal, we recommend the following themes for manuscripts:
• characterization of the dynamic changes and specific functions of diverse cell populations in different phases of aortic adaptation, injury, repair, and remodeling;
• understanding the genetic and epigenetic regulation of aortic cell clonal expansion and phenotypic transitions;
• understanding the crosstalk between aortic wall and other tissues and organs in the TAAD progression;
• uncovering the risks and biomarkers for diagnosis and prediction of aortic rupture or dissection;
• preclinical and translational research for novel targeted therapies in TAAD.
Keywords:
thoracic aortic aneurysm, thoracic aortic dissection, pathophysiology, mechanisms
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.
Thoracic aortic aneurysms and dissections (TAAD) are a life-threatening disease that accounts for a significant proportion of aortic-related deaths. Although hypertension and the presence of a congenital bicuspid aortic valve (BAV) are risk factors for the disease, a genetic predisposition also plays a prominent role in the etiology. Despite its sudden and unpredictable nature, recent advancements in understanding the mechanisms of TAAD have reported that hemodynamic disturbance, inflammatory factors, and metabolic stress contribute greatly to aortic wall modeling. However, effective measures to prevent its onset or progression are currently unavailable.
Therefore, there is a critical need to develop new treatment strategies for TAAD. However, a major barrier to this goal is a poor understanding of the molecular mechanisms that trigger and promote aortic degeneration in sporadic TAAD. The histopathological hallmark of TAAD is aortic medial degeneration, characterized by proteoglycan accumulation (pooling), elastic fiber fragmentation and smooth muscle cell degeneration. This process contributes to vascular remodeling and weakening of the aortic wall, resulting in aortic aneurysm, dissection, and rupture.
This Research Topic aims to address this important unmet clinical need by elucidating the most recent cellular and molecular pathophysiologic mechanisms governing TAAD development, which may lead to pharmaceutical approaches for preventing TAAD progression. The long-term goal of this Research Topic is to improve our understanding of the physiology and pathobiology of aortic wall degeneration and remolding to develop new pharmacological strategies to prevent TAAD formation and progression. This Research Topic will cover the common subtypes of TAAD, including Marfan syndrome, vascular Ehlers-Danlos, Loeys-Dietz, and familial and unifamilial thoracic aortic aneurysm and dissection.
To achieve this goal, we recommend the following themes for manuscripts:
• characterization of the dynamic changes and specific functions of diverse cell populations in different phases of aortic adaptation, injury, repair, and remodeling;
• understanding the genetic and epigenetic regulation of aortic cell clonal expansion and phenotypic transitions;
• understanding the crosstalk between aortic wall and other tissues and organs in the TAAD progression;
• uncovering the risks and biomarkers for diagnosis and prediction of aortic rupture or dissection;
• preclinical and translational research for novel targeted therapies in TAAD.
Keywords:
thoracic aortic aneurysm, thoracic aortic dissection, pathophysiology, mechanisms
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.