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Cardiovascular diseases (CVD) are the number one cause of death worldwide, with atherosclerosis, which is the formation of fatty plaques in the arteries, being the most common underlying cause. The activation of inflammatory events and endothelium dysfunction are crucial for the development and pathophysiology of atherosclerosis. Elevated circulating levels of low-density lipoprotein (LDL) have been associated with severity of atherosclerosis.

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Endothelial Dysfunction Markers in Ovarian Cancer: VTE Risk and Tumour Prognostic Outcomes.

Life (Basel)

December 2024

Molecular Oncology and Viral Pathology Group, Research Centre of IPO Porto (CI-IPOP), Pathology and Laboratory Medicine Department, Clinical Pathology SV/RISE@CI-IPOP (Health Research Network), Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Centre (Porto. CCC), 4200-072 Porto, Portugal.

Ovarian cancer (OC) presents daunting lethality rates worldwide, with frequent late-stage diagnosis and chemoresistance, highlighting the need for improved prognostic approaches. Venous thromboembolism (VTE), a major cancer mortality factor, is partially driven by endothelial dysfunction (ED). ED's pro-inflammatory state fosters tumour progression, suggesting a VTE-independent link between ED and cancer.

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Atherosclerosis (AS) is one of the major catalysts of ischemic cerebrovascular disease, and the death and disease burden from AS and its cerebrovascular complications are increasing. Z-ligustilide (Z-LIG) is a key active ingredient in () and . In this paper, we first introduced LIG's physicochemical properties and pharmacokinetics.

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Vascular regeneration plays a vital role in tissue repair yet is drastically impaired in those with a spinal cord injury (SCI). Pericytes are of great significance as they are entwined with vessel-specific endothelial cells and actively contribute to maintaining the spinal cord's vascular network. Within the neurovascular unit (NVU), subtypes of pericytes characterized by various markers such as PDGFR-β, Desmin, CD146, and NG-2 are involved in vascular regeneration in SCI repair.

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ClC-5 knockout mitigates angiotensin II-induced hypertension and endothelial dysfunction.

Life Sci

December 2024

Department of Pharmacology, Cardiac & Cerebral Vascular Research Center, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou 510080, China. Electronic address:

Aims: Impairment of nitric oxide (NO) production is a major cause of endothelial dysfunction and hypertension. ClC-5 Cl channel is abundantly expressed in the vascular endothelium. However, it remains unclear how it regulates endothelial function.

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