Photodynamic Therapy for Atherosclerosis

Abstract

Atherosclerosis, which currently contributes to 31% of deaths globally, is of critical cardiovascular concern. Current diagnostic tools and biomarkers are limited, emphasizing the need for early detection. Lifestyle modifications and medications form the basis of treatment, and emerging therapies such as photodynamic therapy are being developed. Photodynamic therapy involves a photosensitizer selectively targeting components of atherosclerotic plaques. When activated by specific light wavelengths, it induces localized oxidative stress aiming to stabilize plaques and reduce inflammation. The key advantage lies in its selective targeting, sparing healthy tissues. While preclinical studies are encouraging, ongoing research and clinical trials are crucial for optimizing protocols and ensuring long-term safety and efficacy. The potential combination with other therapies makes photodynamic therapy a versatile and promising avenue for addressing atherosclerosis and associated cardiovascular disease. The investigations underscore the possibility of utilizing photodynamic therapy as a valuable treatment choice for atherosclerosis. As advancements in research continue, photodynamic therapy might become more seamlessly incorporated into clinical approaches for managing atherosclerosis, providing a blend of efficacy and limited invasiveness.

Photodynamic Therapy for Atherosclerosis: Past, Present, and Future

“…Atherosclerosis has evolved as a leading cause of death and disability globally, surpassing communicable diseases to become the top health concern [ 2 , 15 , 16 ]. Fueled by the accumulation of low-density lipoprotein (LDL) and other lipoproteins in arteries, it is primarily driven by inflammation, which orchestrates its progression and outcome [ 17 , 18 , 19 ] ( Figure 1 ). Traditional non-invasive therapeutic interventions have targeted risk factors such as hypertension and hypercholesterolemia [ 20 , 21 ].…”

“…Ref. [ 19 ], Copyright 2024, MDPI. ( ii ) Atherosclerotic lesions develop at the site of vascular endothelium damage, leading to up-regulation of vascular adhesion molecules (e.g., VCAM1, ICAM) and expression of monocyte chemoattractants [monocyte chemoattractant protein-1 (e.g., MCP-1/CCL2)].…”