Vascular Remodeling
Vascular Remodeling - Related Videos
06:55
Assessment of Maternal Vascular Remodeling During Pregnancy in the Mouse Uterus
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Cited by 27 •
2015
This protocol describes a technique to assess changes in the maternal vasculature during pregnancy in mice. Using stereological methods, remodeling of the decidual spiral arteries is assessed quantitatively and the results confirmed qualitatively using immunohistochemistry.
02:54
Nucleosome Remodeling
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2020
Nucleosomes are the basic units of chromatin compaction. Each nucleosome consists of the DNA bound tightly around a histone core, which makes the DNA inaccessible to DNA binding proteins such as DNA polymerase and RNA polymerase. Hence, the fundamental problem is to ensure access to DNA when appropriate, despite the compact and protective chromatin structure. Nucleosome remodeling complex Eukaryotic cells have specialized enzymes called ATP-dependent nucleosome remodeling enzymes. These enzymes...
08:42
A Rat Carotid Balloon Injury Model to Test Anti-vascular Remodeling Therapeutics
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Cited by 8 •
2016
The rat carotid balloon injury model described below allows researchers to evaluate drugs or therapeutics that negate injury-induced arterial hyperplasia. Detailed pre-surgical preparation, surgical procedure, and post-surgical cares of the animal are described.
07:30
In Vitro Model of Physiological and Pathological Blood Flow with Application to Investigations of Vascular Cell Remodeling
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Cited by 6 •
2015
This protocol replicates physiological or pathological blood flow in vitro to aid in determining cell response in disease pathologies. By introducing a pressure damping chamber downstream of a blood pump, blood flow across the vasculature can be recapitulated and imposed on a monolayer of vascular endothelium or a mimetic co-culture.
07:41
A Model of Reverse Vascular Remodeling in Pulmonary Hypertension Due to Left Heart Disease by Aortic Debanding in Rats
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Cited by 2 •
2022
The present protocol describes a surgical procedure to remove ascending-aortic banding in a rat model of pulmonary hypertension due to left heart disease. This technique studies endogenous mechanisms of reverse remodeling in the pulmonary circulation and the right heart, thus informing strategies to reverse pulmonary hypertension and/or right ventricular dysfunction.
FAQs
Changes in blood-flow forces, tissue injury, inflammation, and chemical signals can alter the behavior of endothelial cells and vascular smooth muscle cells. These cells may respond by changing growth, migration, contraction, or communication with the extracellular matrix. The resulting responses can modify vessel diameter, wall thickness, or network organization, linking local stimuli to broader changes in vascular structure and function.
Vascular smooth muscle cells contribute through changes in proliferation, migration, and contraction, while extracellular matrix components influence the vessel’s structural environment. Matrix turnover can change how cells attach, move, and respond to signals. Together, these processes help determine whether a vessel becomes thicker, changes its diameter, or reorganizes its network after altered mechanical or chemical conditions.
Endothelial cells form the vessel lining and respond directly to changes affecting the vascular environment. Their altered behavior can influence neighboring smooth muscle cells and extracellular matrix processes, connecting external stimuli with structural adaptation. Examining endothelial responses therefore helps explain how inflammation, injury, or chemical signals may progress from an initial vascular disturbance to measurable changes in vessel organization and function.
The outcome depends on the combination of hemodynamic forces, injury, inflammation, and chemical signaling, as well as the coordinated responses of endothelial cells, vascular smooth muscle cells, and extracellular matrix components. Changes in growth, migration, contraction, and matrix turnover can produce different structural results. This variation helps explain why remodeling appears differently across cardiovascular diseases and experimental settings.
Studies can examine whether a treatment changes vessel diameter, wall thickness, or the organization of vascular networks, while also assessing cellular behaviors such as growth, migration, and contraction. These outcomes connect drug exposure with structural and functional vascular effects. Evaluating several levels together can show whether a compound influences remodeling directly or alters the signals and cellular processes that drive it.
Researchers examine whether these drug classes modify the cellular and matrix processes associated with vascular remodeling. The relevant question is not only whether vascular function changes, but also whether vessel structure, network organization, cell behavior, or matrix turnover is altered. This approach helps connect pharmacological action with conditions such as hypertension, atherosclerosis, inflammation, or excessive blood-vessel formation.
Remodeling research provides a framework for examining how vessels adapt during disease or after vascular injury. In restenosis, investigators can study structural changes that follow injury, whereas tumor research can focus on altered vascular network organization and blood supply. Pharmacological studies use these contexts to evaluate strategies that influence remodeling, limit harmful vascular changes, or support restoration of vascular integrity.