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Mural Cells: Potential Therapeutic Targets to Bridge Cardiovascular Disease and Neurodegeneration
Alexander Lin1,2, Niridu Jude Peiris1,3, Harkirat Dhaliwal1,3
1Heart Research Institute, Sydney, NSW 2042, Australia.
Insights
Mural cell dysfunction contributes to cardiovascular and neurodegenerative diseases. Targeting conserved signaling pathways offers a dual therapeutic approach for both conditions.
Area of Science:
- Vascular Biology
- Neurodegenerative Diseases
- Cardiovascular Research
Background:
- Mural cells (smooth muscle cells and pericytes) are vital for vascular health, regulating blood pressure and vessel integrity.
- Mural cell dysfunction is implicated in atherosclerosis and increasingly recognized in neurodegenerative diseases like Alzheimer's and Parkinson's.
Purpose of the Study:
- To review mechanisms of atherosclerosis and neurodegeneration, focusing on mural cell plasticity.
- To identify conserved signaling pathways (PDGF, Notch, inflammatory) in both disease types.
- To propose dual-acting therapeutics targeting these conserved pathways.
Main Methods:
- Literature review of mural cell function in cardiovascular and neurodegenerative diseases.
- Analysis of conserved signaling pathways implicated in mural cell plasticity.
- Exploration of therapeutic strategies targeting shared molecular mechanisms.
Main Results:
- Mural cell plasticity is a key mechanism in both atherosclerosis and neurodegeneration.
- Specific signaling pathways, including PDGF, Notch, and inflammatory signaling, are conserved across these conditions.
- These conserved pathways represent potential targets for novel therapeutic interventions.
Conclusions:
- Dysfunctional mural cells contribute to both cardiovascular and neurodegenerative pathologies.
- Targeting conserved mural cell signaling pathways may lead to dual-acting therapies.
- Developing therapeutics with cardio- and neuroprotective qualities is a promising avenue for future research.
Abstract:
Mural cells collectively refer to the smooth muscle cells and pericytes of the vasculature. This heterogenous population of cells play a crucial role in the regulation of blood pressure, distribution, and the structural integrity of the vascular wall. As such, dysfunction of mural cells can lead to the pathogenesis and progression of a number of diseases pertaining to the vascular system. Cardiovascular diseases, particularly atherosclerosis, are perhaps the most well-described mural cell-centric case. For instance, atherosclerotic plaques are most often described as being composed of a proliferative smooth muscle cap accompanied by a necrotic core. More recently, the role of dysfunctional mural cells in neurodegenerative diseases, such as Alzheimer's and Parkinson's disease, is being recognized. In this review, we begin with an exploration of the mechanisms underlying atherosclerosis and neurodegenerative diseases, such as mural cell plasticity. Next, we highlight a selection of signaling pathways (PDGF, Notch and inflammatory signaling) that are conserved across both diseases. We propose that conserved mural cell signaling mechanisms can be exploited for the identification or development of dual-pronged therapeutics that impart both cardio- and neuroprotective qualities.
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