TRPV4 in Cerebral Small Vessel Disease: A key interacting partner.

Area of Science:

• Neuroscience
• Vascular Biology
• Mechanobiology

Background:

• Cerebral small vessel disease (cSVD) is a primary cause of vascular cognitive impairment and dementia.
• cSVD pathogenesis involves neurovascular unit dysfunction, including blood-brain barrier (BBB) impairment, reduced cerebrovascular reactivity, and hypoperfusion.
• Mechanosensitive ion channels in the neurovascular unit are critical for these processes.

Purpose of the Study:

• To review the multifaceted roles of Transient Receptor Potential Vanilloid 4 (TRPV4) channels within the neurovascular unit.
• To explore TRPV4's interactions with molecular partners.
• To discuss the potential contribution of TRPV4 to the pathophysiology of cSVD.

Main Methods:

• Literature review focusing on mechanobiology of cerebral microvessels.
• Analysis of recent evidence on TRPV4's physiological and pathological roles.
• Synthesis of findings related to TRPV4 and cSVD mechanisms.

Main Results:

• TRPV4 channels regulate key physiological functions: vascular tone, angiogenesis, BBB integrity, and neuroinflammation.
• TRPV4 is implicated in pathological processes including cerebrovascular remodeling, impaired reactivity, and BBB dysfunction.
• TRPV4 channels are expressed in cells of the neurovascular unit, suggesting a direct role in cSVD.

Conclusions:

• TRPV4 plays a significant role in the normal functioning of the neurovascular unit.
• Dysregulation of TRPV4 contributes to pathological changes observed in cSVD.
• Targeting TRPV4 may offer a therapeutic strategy for managing cSVD and related cognitive decline.