Mechanism of Hypoxia-Mediated Smooth Muscle Cell Proliferation Leading to Vascular Remodeling

Abstract

Vascular remodeling refers to changes in the size, contraction, distribution, and flow rate of blood vessels and even changes in vascular function. Vascular remodeling can cause cardiovascular and cerebrovascular diseases. It can also lead to other systemic diseases, such as pulmonary hypertension, pulmonary atherosclerosis, chronic obstructive pulmonary disease, stroke, and ascites of broilers. Hypoxia is one of the main causes of vascular remodeling. Prolonged hypoxia or intermittent hypoxia can lead to loss of lung ventilation, causing respiratory depression, irregular respiratory rhythms, and central respiratory failure. Animals that are unable to adapt to the highland environment are also prone to sustained constriction of the small pulmonary arteries, increased resistance to pulmonary circulation, and impaired blood circulation, leading to pulmonary hypertension and right heart failure if they live in a highland environment for long periods of time. However, limited studies have been found on the relationship between hypoxia and vascular remodeling. Therefore, this review will explore the relationship between hypoxia and vascular remodeling from the aspects of endoplasmic reticulum stress, mitochondrial dysfunction, abnormal calcium channel, disordered cellular metabolism, abnormal expression of miRNA, and other factors. This will help to understand the detailed mechanism of hypoxia-mediated smooth muscle cell proliferation and vascular remodeling for the better treatment and management of diseases due to vascular remodeling.

Vascular Calcification: Molecular Networking, Pathological Implications and Translational Opportunities

“…Hypoxia within the vascular microenvironment can trigger signaling cascades that contribute to the differentiation of VSMCs toward a chondrogenic phenotype [ 59 ]. The mechanisms underlying VSMC calcification under hypoxic conditions require either hypoxia-inducible factor (HIF) activation or the production of mitochondrial-derived reactive oxygen species (ROS) [ 60 , 61 ]. High levels of inorganic phosphate (Pi) increase VSMC migration and calcification and are related to impaired Pi/calcium balance and miR-223 involvement, whereas TGF-β/Smad3 signaling plays an inhibitory role in Pi-induced VSMC calcification [ 62 , 63 , 64 ].…”

Unlocking the Full Potential of SGLT2 Inhibitors: Expanding Applications beyond Glycemic Control

“…In cardiovascular diseases, IL-6 and TNF are involved in the pathogenesis of atherosclerosis, myocardial infarction, and heart failure. Elevated levels of IL-6 or TNF are associated with an increased risk of cardiovascular events and a worse prognosis in patients with heart failure [ 59 ]. Furthermore, in cardiovascular diseases, collagen is involved in the regulation of tissue repair and remodeling, particularly in response to injury or stress.…”

The Inhibitory Activity of Natural Products to Xanthine Oxidase

“…Natural products are valuable biological resources with wide applications. [97][98][99][100][101][102][103][104][105][106][107][108][109][110][111][112][113][114][115][116] These natural products of extracted mixture or monomer showed good biological activity in the screening of anti-gout activity in vitro, which has the value for further research of gout treatment. In this review, studies on anti-gout activities were mainly summarized from the aspects of active components and monomers of natural products.…”