Mechanical stress-initiated signal transduction in vascular smooth muscle cells in vitro and in vivo.
Increasing evidence has been demonstrated that hypertension-initiated abnormal biomechanical stress is strongly associated with cardio-/cerebrovascular diseases e.g. atherosclerosis, stroke, and heart failure, which is main cause of morbidity and mortality. How the cells in the cardiovascular system sense and transduce the extracellular physical stimuli into intracellular biochemical signals is a crucial issue for understanding the mechanisms of the disease development. Recently, collecting data derived from our and other laboratories showed that many kinds of molecules in the cells such as receptors, ion channels, caveolin, G proteins, cell cytoskeleton, kinases and transcriptional factors could serve as mechanoceptors directly or indirectly in response to mechanical stimulation implying that the activation of mechanoceptors represents a non-specific manner. The sensed signals can be further sorted and/or modulated by processing of the molecules both on the cell surface and by the network of intracellular signaling pathways resulting in a sophisticated and dynamic set of cues that enable cardiovascular cell responses. The present review will summarise the data on mechanotransduction in vascular smooth muscle cells and formulate a new hypothesis, i.e. a non-specific activation of mechanoceptors followed by a variety of signal cascade activation. The hypothesis could provide us some clues for exploring new therapeutic targets for the disturbed mechanical stress-initiated diseases such as hypertension and atherosclerosis.
Li
Chaohong
C
Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong 510080, China.
Xu
Qingbo
Q
D000818:Animals; D006801:Humans; D040542:Mechanotransduction, Cellular; D009131:Muscle, Smooth, Vascular / Q000166:cytology; D032389:Myocytes, Smooth Muscle / Q000378:metabolism*; D013314:Stress, Mechanical; D014652:Vascular Diseases / Q000378:metabolism