What is it about?
Hypertension can lead to arteriosclerosis through alterations in the structure of blood vessel walls known as “vascular remodeling.” Why and how hypertension triggers vascular remodeling is not entirely clear. So far, several studies have shown that macrophages are involved in the transformation. Specifically, the macrophages accumulate within blood vessel walls from outside the vessels and cause chronic inflammation. However, the underlying mechanism that orchestrates this process remains unknown. In this study, we unveiled a molecular pathway for the development of arteriosclerosis for the first time. This could pave the way to better medication for preventing and treating hypertension and arteriosclerosis.
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Why is it important?
We identified a detailed molecular mechanism by which high pressure and subsequent Ca2+ influx through calcium channels in vascular smooth muscle cells activate certain transcription factors and enzymes. Importantly, the transcription of various genes related to chemotaxis was triggered by high pressure. This helped explain the accumulation of macrophages in blood vessel walls. Additionally, the vascular remodeling was promoted by the activation of the molecular pathway. Taken together, our results explain how high pressure applied to vascular smooth muscle can modulate macrophage migration and subsequent inflammation, altering the vascular structure.
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This page is a summary of: A molecular complex of Ca
1.2/CaMKK2/CaMK1a in caveolae is responsible for vascular remodeling via excitation–transcription coupling, Proceedings of the National Academy of Sciences, April 2022, Proceedings of the National Academy of Sciences, DOI: 10.1073/pnas.2117435119.
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