Shi J, Yang Y, Cheng A, Xu G, He F. Metabolism of vascular smooth muscle cells in vascular diseases. Atherosclerotic plaques are characterized by the accumulation of cholesterol crystals in the arterial wall, a fibrous cap rich in extracellular matrix produced by vascular smooth muscle cells (VSMCs) and infiltration of immune cells (such as monocytes-macrophages, T cells, and mast cells) 3, 4. Photoelasticity-based evaluation of cellular contractile force for phenotypic discrimination of vascular smooth muscle cells. Photoelasticity-based evaluation of cellular contractile force for phenotypic discrimination of vascular smooth muscle cells Coronary artery bypass grafting, intimal hyperplasia, phenotypic switching, vascular smooth muscle cells, vein graft failure Zargham R, Touyz RM, Thibault G. Alpha 8 integrin overexpression in de‐differentiated vascular smooth muscle cells attenuates migratory activity and restores the characteristics of the differentiated phenotype. Generation and comparative analysis of an Itga8‐CreER (T2) mouse with preferential activity in vascular smooth muscle cells. Shioi A, Nishizawa Y, Jono S, Koyama H, Hosoi M, Morii H. Beta‐glycerophosphate accelerates calcification in cultured bovine vascular smooth muscle cells.

Discover the latest articles, books and news in related subjects, suggested using machine learning. New to the series this time around are Propaganda Missions, which give you a limited amount of time to sneak in and complete tasks. Like previous installments, stealth and sniping from afar are key to your success. With time-sensitive objectives, players must sneak, snipe and shoot, taking down enemies under certain conditions to complete their mission. Harry Hawker, agent of the Special Operations Executive (SOE), takes the lead role for the first time in the series as he discovers an insidious new Wunderwaffe—something so powerful, it guarantees the Nazis would win the war. Receive real-time notifications about updates and replies on your message board. Time flies when you are thrust into the French countryside in order to prevent wartime disaster.

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Cholesterol‐induced phenotypic modulation of smooth muscle cells to macrophage/fibroblast‐like cells is driven by an unfolded protein response. Transdifferentiation of mouse aortic smooth muscle cells to a macrophage‐like state after cholesterol loading. Low LAL (lysosomal acid lipase) expression by smooth muscle cells relative to macrophages as a mechanism for arterial foam cell formation. Contribution of intimal smooth muscle cells to cholesterol accumulation and macrophage‐like cells in human atherosclerosis. BMAL1 modulates smooth muscle cells phenotypic switch towards fibroblast‐like cells and stabilizes atherosclerotic plaques by upregulating YAP1.

Rapamycin (mTOR inhibitor) failed to reverse these changes, indicating a potential role between impaired autophagy mediated by the KLF4-dependent mTOR signaling pathway and the VSMC phenotypic remodeling . Leucine supplementation activates the SIRT1-Foxo1 pathway through the Slc3a2/Slc7a5 transporter, inhibiting the transformation of VSMC to a synthetic phenotype, vascular inflammatory response, and ROS generation during aging . At the same time, single-cell RNA sequencing and microarray analysis found that glutamate metabolism-related enzymes Glutamate-Ammonia Ligase and Glutaminase (GLS) and glutamate receptor subunits GRIA1 and GRIA2 were highly expressed in VSMCs. The latest study found that glutamine and serine as anaplerosis of the TCA cycle increased in unstable plaques . Adipokine stimulation upregulates CD36, a key fatty acid transporter in VSMCs, resulting in enhanced fatty acid uptake and lipid deposition, ERK pathway activation, and subsequent VSMC proliferation and inflammatory responses .

Non-coding RNAs, important epigenetic regulators, primarily include microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs). Targeting key molecules within the NF-κB pathway—such as circACTA2 and HMGB1/2—may help preserve the contractile phenotype of VSMCs and offers promising therapeutic strategies for vascular remodeling–related diseases. A variety of stimuli can activate this pathway in VSMCs, promoting their transition to a synthetic phenotype and accelerating pathological remodeling. Elucidating its molecular mechanisms not only enhances our understanding of vascular remodeling but also provides a promising foundation for the development of targeted therapeutic strategies aimed at preventing vascular graft failure and related pathologies. It involves the integration of multiple signaling pathways (MAPK, mTOR, NF-κB, TGF-β) and a complex network of non-coding RNAs (miRNAs, lncRNAs, circRNAs), which ooosch online casino collectively orchestrate the transition from a contractile to a synthetic phenotype. The mechanism is initiated by endothelial dysfunction and amplified by the key driver PDGF-BB. A thorough understanding of PDGF-BB–mediated signaling pathways may provide essential theoretical support for the development of targeted therapies to prevent VGF.

1 Role Of Endothelial Cells (ecs) Dysfunction

Furthermore, the contribution of endogenous progenitor cells in the tunica media or adventitia remains to be further verified. In addition, VSMCs are thought to achieve phenotype switching through selective expression of marker genes. In ApoE−/− mice, NFATc1 deletion reduced CD137L-induced neointima formation . Chappell et al. showed that VSMCs-derived cells in the neointima of AS were usually formed by clonal expansion of a few VSMCs in tunica media . Another study showed that VSMC-derived foam cells carried a higher cholesterol burden than leukocyte derived foam cells . A recent study showed that in advanced coronary atherosclerotic plaque, 50% of foam cells express the VSMCs marker ACTA2. A recent lineage tracing experiment exploring the origin of foam cells in AS showed that manifold VSMCs, which should be quiescent in the tunica media, migrated to tunica intima and transform to macrophage-like VSMCs . Since vascular calcification occurs only in arteries but not in veins, it suggests that VSMCs, the specific component of arteries, play an irreplaceable role in arterial calcification.

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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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