How Vascular Smooth Muscle Cell Phenotype Switching Contributes To Vascular Disease Cell Communication And Signaling Springer Nature Link

Intimal smooth muscle cells of porcine and human coronary artery express S100A4, a marker of the rhomboid phenotype in vitro. Single‐cell genomics reveals a novel cell state during smooth muscle cell phenotypic switching and potential therapeutic targets for atherosclerosis in mouse and human. Cao G, Xuan X, Hu J, Zhang R, Jin H, Dong H. How vascular smooth muscle cell phenotype switching contributes to vascular disease. ACTA indicates α‐smooth muscle actin; CArG, CC(A/T‐rich)6GG cis‐regulating element; Itga8, integrin alpha 8; Myh11, myosin heavy chain 11; SRF, serum response factor; Tagln, transgelin; and VSMC, vascular smooth muscle cell. Some potential markers include platelet‐derived growth factor receptor beta and S100A4.13, 21, 22 Of note, the contraction mechanism of myofibroblasts is different from that of VSMCs.52, 53 Thus, it is possible that analyzing the contractile characteristics can help distinguish myofibroblast‐like VSMCs from VSMCs. VSMCs phenotype switching provides a new perspective for understanding the pathogenesis of vascular diseases. Great progress has been made in the study of the role of VSMCs phenotype transformation in vascular diseases in the past 20 years.

PDGF-BB, a key member of the PDGF family, is a peptide growth factor with diverse biological functions. In vitro studies have demonstrated that venous VSMCs are smaller, spindle-shaped, and exhibit enhanced proliferative and migratory potential. Commonly used vascular grafts in CABG include the left internal mammary artery (LIMA), radial artery (RA), and great saphenous vein (GSV). Check if you have access through your login credentials or your institution to get full access on this article. If you have the appropriate software installed, you can download article citation data to the citation manager of your choice. Authors of the article cited in the comment will be invited to reply, as appropriate. ELetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Expression and promoter analysis of a highly restricted integrin alpha gene in vascular smooth muscle.

In the PKG-independent pathway, 6-aminonicotinamide can directly stimulate the expression of MYOCD/miR-143 and downregulate the synthetic phenotype-responsive SRF-ELK1 complex to maintain the contractile phenotype. HnRNPA1 is a key regulator of PKM2 mRNA splicing, which can promote PKM2 expression and glycolysis. PKM2 is a key enzyme in the last step of glycolysis, converting phosphoenolpyruvate to pyruvate and supplying ATP . Acetyl CoA and citrate produced by glycolysis provide fuel for de novo fatty acid synthesis . At the same time, upregulation of PFKFB3 builds a carbon atom-sharing bridge between glycolysis ooosch slots and fatty acid synthesis. Metabolic reprogramming of plaques provide clues to changes in the metabolic pattern of cells within the plaque. In high-risk plaques, glycolysis and pentose phosphate pathway (PPP) are enhanced, fatty acid oxidation (FAO) is reduced, and amino acid anaplerosis is increased 5,6,7. Vascular smooth muscle cell metabolic reprogramming and phenotypic remodeling in atherosclerosis

Smooth Muscle Cell Differentiation: Mechanisms And Models For Vascular Diseases

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. This approach offers the potential for sustained inhibition and even regression of IH. This shift provides a scientific basis for the advancement of cardiovascular disease therapies. Currently, the primary pharmacological agents include microtubule stabilizers (e.g., paclitaxel-based drugs) and mTOR signaling inhibitors (e.g., rapamycin-based drugs). EDIs, which are buffer solutions developed based on the GALA formula (containing reduced glutathione, L-ascorbic acid, and L-arginine), exhibit antioxidant properties, scavenge free radicals, and support eNOS activity (95, 96).

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Buffer solutions—such as the University of Wisconsin solution, TiProtec, and He solution—can better maintain ion homeostasis and physiological pH. These solutions provide superior protection of endothelial structure and function compared to AWB and normal saline (93). The proposed protective mechanisms include the preservation of eNOS activity, which is abundantly expressed in the adventitia, and the retention of perivascular adipose tissue markers such as leptin and adiponectin (85, 86). These approaches provide a diversified portfolio for improving vein graft patency. Further elucidation of their roles may not only deepen our understanding of IH but also provide theoretical foundations and therapeutic targets for developing effective intervention strategies. To facilitate comparison and provide an integrated overview of the evidence discussed above, representative studies describing non-coding RNAs-mediated regulation of VSMCs phenotypic switching, including molecular targets and functional consequences, are summarized in Table 2. These molecules participate in the regulation of VSMCs phenotypic switching through intricate molecular mechanisms and play essential roles in the onset and progression of cardiovascular diseases (Figure 2).

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Malonyl-CoA decarboxylase (MCD) is an endogenous inhibitor of CPT1 and a key regulatory enzyme of FAO . As a result, FAO is suppressed, causing accumulation of intracellular long-chain fatty acids and reduced palmitate oxidation activity, ultimately enhancing VSMC proliferation and migration . In Elovl6-/- mice, the formation of new intima is significantly reduced, the number of Ki-67-positive cells and the expression of α-SMA and SM22α are reduced. The latest study found that Elovl6 co-localizes with α-SMA -positive cells during vascular injury. The energy produced by aerobic glycolysis can be provided by FAO, and the activity of glycolysis is regulated by the feedback of FAO metabolites . In TRAP1-knockout rats, acetyl-CoA and citrate were increased, and the expression levels of senescence markers (P53, P21, and P16) and H4K12la in VSMCs were decreased, while lipid accumulation, plaque area, and necrotic core size in the aorta were reduced . In addition, SM22α can synergistically enhance G6PD activity, stimulate the PPP to increase NADPH production, maintain GSH homeostasis, and promote VSMC proliferation and migration . Immunoprecipitation revealed that the N-terminal domain of G6PD interacts with VDAC1 and competes with Bax for binding to VDAC1, alleviating VSMC apoptosis by reducing VDAC1 oligomerization and maintaining the synthetic phenotype of VSMC .

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Changes in retardation with time when the chemical reagent was applied to the cell to alter the cellular contraction state. Under the assumption that the refractive index stays constant, retardation measurements provide information on the mechanical state. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher. The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice.