Targeting VCAM-1: a therapeutic opportunity for vascular damage

ABSTRACT

Introduction

The vascular cell adhesion molecule (VCAM-1) is a transmembrane sialoglycoprotein detected in activated endothelial and vascular smooth muscle cells involved in the adhesion and transmigration of inflammatory cells into damaged tissue. Widely used as a pro-inflammatory marker, its potential role as a targeting molecule has not been thoroughly explored.

Areas covered

We discuss the current evidence supporting the potential targeting of VCAM-1 in atherosclerosis, diabetes, hypertension and ischemia/reperfusion injury.

Expert opinion

There is emerging evidence that VCAM-1 is more than a biomarker and may be a promising therapeutic target for vascular diseases. While there are neutralizing antibodies that allow preclinical research, the development of pharmacological tools to activate or inhibit this protein are required to thoroughly assess its therapeutic potential.

KEYWORDS:

• VCAM-1
• inflammation
• vascular damage
• cardiovascular diseases
• therapeutic target

Article highlights

• VCAM-1 is an adhesion molecule induced by inflammatory cytokines that mediate the adhesion and transmigration of leukocytes from blood into the injury site through blood vessels.

• VCAM-1 expression is increased in activated endothelial and vascular smooth muscle cells in atherosclerosis, hypertension, and diabetes.

• The development of novel strategies to modulate the activity and expression of VCAM- is required to evaluate its molecular contribution to the development of cardiovascular disease. VCAM-1 action can be blocked using a neutralizing antibody to reduce hypertension.

This box summarizes key points contained in the article.

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This work was funded by Agencia Nacional de Investigacion y Desarrollo (ANID): PhD Fellowship 21180537 (MFT), and grants FONDECYT 1200490 (SL) and FONDAP 15130011 (MCh, SL).