Smooth muscle cells constitute a heterogeneous collection of effector cells that, by virtue of both their constituency in blood vessels and presence as primary parenchymal cells in diverse tissues, affect the function of all organs. Thus, perhaps it is not surprising that alterations in, and/or dysfunction of, smooth muscle cells are quite common, and responsible, at least in part, for the morbidity and mortality associated with a very wide range of human diseases. These facts point to the necessity for improved understanding of the mechanism(s) governing the control of myocyte contractility (i.e., tone). Such understanding has been rapidly forthcoming in recent years, and has indicated that in many smooth muscle cell types intercellular communication through gap junctions acts in concert with nonjunctional (K+) ion channels to make important contributions to the control of myocyte tone and tissue homeostasis in physiologically diverse organs. Intercellular communication through connexin43-derived gap junction channels and K+ flux through the KCa and KATP channel subtypes, in particular, appear to play prominent roles in this process. The goal of this report, therefore, is to review the data concerning junctional and nonjunctional ion channels on the detrusor myocytes of the urinary bladder, as well as on the specialized vascular myocytes of the corpus cavernosum. The choice of an excitable (i.e., bladder detrusor myocytes) and nonexcitable (i.e., corporal smooth muscle) smooth muscle cell type ensures that the discussion will at least encompass consideration of a large portion of the spectrum of physiological possibilities for the participation of junctional and nonjunctional ion channels in the initiation, maintenance and modulation of smooth muscle tone. A central thesis of this communication is that detailed knowledge of the myocyte- and tissue-specific properties of K+ channels and gap junctions will likely lead to the improved understanding and treatment of human smooth muscle diseases/disorders.

Download full-text PDF

Source
http://dx.doi.org/10.2174/1389450013348894DOI Listing

Publication Analysis

Top Keywords

smooth muscle
32
gap junctions
12
improved understanding
12
nonjunctional ion
12
ion channels
12
channels gap
8
smooth
8
muscle
8
muscle cells
8
control myocyte
8

Similar Publications

An uncommon and recently identified Müllerian anomaly is the accessory cavitated uterine mass (ACUM). It is distinguished by the presence of a noncommunicating auxiliary cavity inside the uterus, located near and surrounded by uterine smooth muscle, and bordered by functioning endometrium beneath the round ligament's insertion, with a perfectly healthy uterus, ovaries, tubes, and cavity. Given that it is a congenital ailment with a persistent Müllerian duct at the level of the round ligament, primarily resulting from gubernaculum dysfunction, it usually manifests clinically as childhood dysmenorrhea in girls.

View Article and Find Full Text PDF

Background: Previous studies have suggested that changes in the composition of the extracellular matrix (ECM) play a significant role in the development of ligamentum flavum hypertrophy (LFH) and the histological differences between the ventral and dorsal layers of the hypertrophied ligamentum flavum. Although LFH is associated with increased fibrosis in the dorsal layer, comprehensive research exploring the characteristics of the ECM and its mechanical properties in both regions is limited. Furthermore, the distribution of fibrosis-associated myofibroblasts within LFH remains poorly understood.

View Article and Find Full Text PDF

The pathophysiological relationship between wound healing impairment and diabetes is an intricate process. Burn injury among diabetes patients leads to neurological, vascular, and immunological abnormalities along with impaired activities of cell proliferation, collagen production, growth factors, and cytokine activities with huge bacterial infestation. In our study, we aimed to achieve a burn wound dressing material with the help of electrospun Chitosan/Polyethylene oxide/Rosmarinic acid (CS/PEO/RA) nanofibers.

View Article and Find Full Text PDF

SERCA2 dysfunction accelerates angiotensin II-induced aortic aneurysm and atherosclerosis by induction of oxidative stress in aortic smooth muscle cells.

J Mol Cell Cardiol

January 2025

School of Pharmaceutical Sciences, Chongqing University, Chongqing 401331, China; State Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD), Harbin Medical University, China; Chongqing Key Laboratory of New Drug Delivery System, Chongqing 400038, China. Electronic address:

Background And Aim: Our previous research indicates that sarcoplasmic/endoplasmic reticulum calcium ATPase 2 (SERCA2) dysfunction facilitates the phenotypic transformation of aortic smooth muscle cells (ASMCs) and intensifies aortic aneurysm through the regulation of calcium-dependent pathways and endoplasmic reticulum stress. Our hypothesis is that additional mechanisms are involved in aortic aneurysm and atherosclerosis induced by SERCA2 dysfunction from the perspective of ASMC phenotypic transformation.

Methods & Results: In SERCA2 dysfunctional mice and their control littermates, ASMCs were isolated to analyze protein expression and cell functions, and angiotensin II was infused into these mice that were backcrossed into LDL receptor deficient background to induce aortic aneurysm and atherosclerosis.

View Article and Find Full Text PDF

RGFP966 inhibits palmitic acid induced VSMCs phenotypic transition by targeting ATGL.

Biochim Biophys Acta Mol Cell Biol Lipids

January 2025

Department of Pharmacy, The Third Xiangya Hospital, Central South University, Changsha 410013, China. Electronic address:

Background: The phenotypic switch of vascular smooth muscle cells (VSMCs) underlies the pathology of many cardiovascular diseases. Histone deacetylase 3 (HDAC3) is reported to upregulate in several cardiovascular diseases. RGFP966 is a highly selective HDAC3 inhibitor.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!