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Published on: June 7, 2013
Signaling pathways in vascular function and hypertension: molecular mechanisms and therapeutic interventions
Jun Ma1, Yanan Li1, Xiangyu Yang1
1Department of Cardiology, West China Hospital, Sichuan University, No. 37, Guo Xue District, Chengdu, Sichuan, 610041, People's Republic of China.
Insights
Hypertension, a major global health concern, is difficult to treat due to complex vascular dysfunction. This review explores key signaling pathways in vascular cells that contribute to hypertension and potential therapeutic targets.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Physiology
Background:
- Hypertension is a leading cause of premature death globally, posing a significant public health challenge.
- Despite extensive research, the complex mechanisms underlying hypertension and vascular dysfunction remain incompletely understood.
- Vascular function, encompassing elasticity, caliber, and reactivity, directly impacts blood pressure and is crucial for clinical management.
Purpose of the Study:
- To comprehensively review signaling pathways involved in vascular function regulation and hypertension.
- To elucidate the molecular mechanisms in endothelial and smooth muscle cells underlying vascular dysfunction.
- To summarize current and potential future hypertension treatments targeting vascular signaling pathways.
Main Methods:
- Review of existing literature on molecular signaling pathways in vascular biology and hypertension.
- Analysis of pathways including calcium, NO-NOsGC-cGMP, vascular remodeling, renin-angiotensin-aldosterone system, oxidative stress, and immunity/inflammation.
- Synthesis of information on therapeutic strategies targeting these pathways for hypertension management.
Main Results:
- Identified key signaling pathways in vascular endothelial and smooth muscle cells critical for blood pressure regulation.
- Detailed the molecular alterations in these pathways that contribute to vascular dysfunction and hypertension development.
- Highlighted the role of upstream pathways like the renin-angiotensin-aldosterone system and oxidative stress in hypertension.
Conclusions:
- Understanding the intricate signaling pathways in vascular cells is essential for deciphering hypertension's complexity.
- Targeting specific molecular pathways offers promising avenues for novel hypertension therapies.
- Further research into these pathways could lead to more effective clinical interventions for managing blood pressure.
Abstract:
Hypertension is a global public health issue and the leading cause of premature death in humans. Despite more than a century of research, hypertension remains difficult to cure due to its complex mechanisms involving multiple interactive factors and our limited understanding of it. Hypertension is a condition that is named after its clinical features. Vascular function is a factor that affects blood pressure directly, and it is a main strategy for clinically controlling BP to regulate constriction/relaxation function of blood vessels. Vascular elasticity, caliber, and reactivity are all characteristic indicators reflecting vascular function. Blood vessels are composed of three distinct layers, out of which the endothelial cells in intima and the smooth muscle cells in media are the main performers of vascular function. The alterations in signaling pathways in these cells are the key molecular mechanisms underlying vascular dysfunction and hypertension development. In this manuscript, we will comprehensively review the signaling pathways involved in vascular function regulation and hypertension progression, including calcium pathway, NO-NOsGC-cGMP pathway, various vascular remodeling pathways and some important upstream pathways such as renin-angiotensin-aldosterone system, oxidative stress-related signaling pathway, immunity/inflammation pathway, etc. Meanwhile, we will also summarize the treatment methods of hypertension that targets vascular function regulation and discuss the possibility of these signaling pathways being applied to clinical work.
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