Biomechanical signal communication in vascular smooth muscle cells

Zhou, Yan; Liu, Shuying; Li, Chaohong

doi:10.1007/s12079-020-00576-1

Cited by 19 publications

(14 citation statements)

References 174 publications

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“…Among vascular cells SMC proliferation is crucial in atherogenesis, and cyclical stretching mediated by Piezo1 is commonly known to raise the SMC proliferation (Figures 3 & 4). Piezo1is crucial for sensing and transduction of mechanical cues, including shear stress [14,34] and stretching [98,110,[117][118][119][120][121], stretching was shown to work in synergy with OxLDL (oxidized lipoprotein) and norepinephrine in aggravating SMC proliferating by triggering of (ERK) signaling in both mice and rabbits [107,[122][123][124][125]. Piezo1 is necessary for shear sensing [34,126,127], and shear stress was also known to speed up and regulate SMC proliferation via several mechanisms including MMP-2, MMP-9, PDGF, and the trigger of phosphatidylinositol 3 kinase (PI3K)protein kinase B, ERK1/2, Akt signaling [128].…”

Section: Proliferationmentioning

confidence: 99%

Emerging Piezo1 signaling in inflammation and atherosclerosis; a potential therapeutic target

Shinge¹,

Zhang²,

Din³

et al. 2022

Int. J. Biol. Sci.

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Purpose of Review: Atherosclerosis is the principal cause of cardiovascular diseases (CVDs) which are the major cause of death worldwide. Mechanical force plays an essential role in cardiovascular health and disease. To bring the awareness of mechanosensitive Piezo1 role in atherosclerosis and its therapeutic potentials we review recent literature to highlight its involvement in various mechanisms of the disease. Recent Findings: Recent studies reported Piezo1 channel as a sensor, and transducer of various mechanical forces into biochemical signals, which affect various cellular activities such as proliferation, migration, apoptosis and vascular remodeling including immune/inflammatory mechanisms fundamental phenomenon in atherogenesis. Summary: Numerous evidences suggest Piezo1 as a player in different mechanisms of cell biology, including immune/inflammatory and other cellular mechanisms correlated with atherosclerosis. This review discusses mechanistic insight about this matter and highlights the drugability and therapeutic potentials consistent with emerging functions Piezo1 in various mechanisms of atherosclerosis. Based on the recent works, we suggest Piezo1 as potential therapeutic target and a valid candidate for future research. Therefore, a deeper exploration of Piezo1 biology and translation towards the clinic will be a novel strategy for treating atherosclerosis and other CVDs.

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Section: Proliferationmentioning

confidence: 99%

Emerging Piezo1 signaling in inflammation and atherosclerosis; a potential therapeutic target

Shinge¹,

Zhang²,

Din³

et al. 2022

Int. J. Biol. Sci.

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“…SIRT1 promotes both the activation of forkhead transcription factor 3a (Foxo3a) and inhibition of Foxo4, resulting in a more contractile phenotype on stretched rat SMCs than the static controls [ 44 ]. The role of mechanical force-induced epigenetic modifications in vascular gene expression has been extensively studied in endothelial cells [ 98 ] and less in SMCs [ 99 ]. In rat smooth muscle cells, physiological stretching for 48 h (10%, 1 Hz) significantly regulated the expression of histone deacetylases, particularly HDAC3, 4, and 7, compared to static cultured cells ( Figure 3 A).…”

Section: Smooth Muscle Cell Mechanotransductionmentioning

confidence: 99%

“…These changes in the expression of stretched cells accompanied a reduced migration compared to the static controls [ 100 ]. The other mechanisms by which shear stress and stretch induce the expression of epigenetic factors to modulate SMC functions have been recently reviewed [ 99 ].…”

Section: Smooth Muscle Cell Mechanotransductionmentioning

confidence: 99%

The Phenotypic Responses of Vascular Smooth Muscle Cells Exposed to Mechanical Cues

Jensen

Bentzon

Albarrán-Juárez

2021

Cells

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During the development of atherosclerosis and other vascular diseases, vascular smooth muscle cells (SMCs) located in the intima and media of blood vessels shift from a contractile state towards other phenotypes that differ substantially from differentiated SMCs. In addition, these cells acquire new functions, such as the production of alternative extracellular matrix (ECM) proteins and signal molecules. A similar shift in cell phenotype is observed when SMCs are removed from their native environment and placed in a culture, presumably due to the absence of the physiological signals that maintain and regulate the SMC phenotype in the vasculature. The far majority of studies describing SMC functions have been performed under standard culture conditions in which cells adhere to a rigid and static plastic plate. While these studies have contributed to discovering key molecular pathways regulating SMCs, they have a significant limitation: the ECM microenvironment and the mechanical forces transmitted through the matrix to SMCs are generally not considered. Here, we review and discuss the recent literature on how the mechanical forces and derived biochemical signals have been shown to modulate the vascular SMC phenotype and provide new perspectives about their importance.

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“…Many mechanosensors were identified on VSMCs to sense the surrounding mechanical stimuli such as membrane-like receptors, ion channels and pumps, glycocalyx, primary cilium, and integrins [ 114 , 115 ]. These mechanosensors could transmit signals from the surroundings to affect the SMC phenotype as an adaptive response [ 116 ]. Hu et al demonstrated that the adaptor molecules of membrane mechanosensors are inactive in the quiescent SMC.…”

Section: The Effect Of Hemodynamics On Smooth Muscle Cell Phenotype During Arteriogenesismentioning

confidence: 99%

Role of Vascular Smooth Muscle Cell Phenotype Switching in Arteriogenesis

Ashraf

Zen

2021

IJMS

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Arteriogenesis is one of the primary physiological means by which the circulatory collateral system restores blood flow after significant arterial occlusion in peripheral arterial disease patients. Vascular smooth muscle cells (VSMCs) are the predominant cell type in collateral arteries and respond to altered blood flow and inflammatory conditions after an arterial occlusion by switching their phenotype between quiescent contractile and proliferative synthetic states. Maintaining the contractile state of VSMC is required for collateral vascular function to regulate blood vessel tone and blood flow during arteriogenesis, whereas synthetic SMCs are crucial in the growth and remodeling of the collateral media layer to establish more stable conduit arteries. Timely VSMC phenotype switching requires a set of coordinated actions of molecular and cellular mediators to result in an expansive remodeling of collaterals that restores the blood flow effectively into downstream ischemic tissues. This review overviews the role of VSMC phenotypic switching in the physiological arteriogenesis process and how the VSMC phenotype is affected by the primary triggers of arteriogenesis such as blood flow hemodynamic forces and inflammation. Better understanding the role of VSMC phenotype switching during arteriogenesis can identify novel therapeutic strategies to enhance revascularization in peripheral arterial disease.

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Biomechanical signal communication in vascular smooth muscle cells

Cited by 19 publications

References 174 publications

Emerging Piezo1 signaling in inflammation and atherosclerosis; a potential therapeutic target

Emerging Piezo1 signaling in inflammation and atherosclerosis; a potential therapeutic target

The Phenotypic Responses of Vascular Smooth Muscle Cells Exposed to Mechanical Cues

Role of Vascular Smooth Muscle Cell Phenotype Switching in Arteriogenesis

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