# Progress in the Cross-Organ Biomarker oxLDL in Promoting Pathological Neovascular Diseases

## TL;DR

This paper reviews how oxidized LDL contributes to blood vessel-related diseases across multiple organs and suggests it could be a key target for treatment.

## Contribution

The paper integrates molecular mechanisms of oxLDL's role in promoting neovascular diseases across multiple organs.

## Key findings

- oxLDL accumulates in disease-specific microenvironments and activates inflammatory pathways.
- oxLDL modulates macrophage and endothelial cell function to drive pathological angiogenesis.
- oxLDL acts as a systemic biomarker linked to chronic inflammation and tissue damage in multiple diseases.

## Abstract

Neovascular diseases, such as neovascular ophthalmopathy, atherosclerosis, and tumors, are characterized by pathological angiogenesis, leading to the formation of leaky, tortuous, and immature blood vessels, often accompanied by chronic inflammation and tissue damage. Among the multiple drivers of angiogenesis in these conditions, the role of oxidized low-density lipoprotein (oxLDL) has garnered increasing attention. Formed from low-density lipoprotein (LDL) under oxidative stress, oxLDL acts as a cross-organ biomarker that systemically impacts multiple organs via the circulatory system, exerting a pivotal pro-angiogenic effect. This review focuses on elucidating the common molecular mechanisms by which oxLDL and its downstream lipid peroxidation products accumulate in disease-specific microenvironments. This accumulation activates inflammatory and oxidative stress pathways in macrophages and endothelial cells, modulating their functional reprogramming and thereby driving pathological neovascularization. Our aim is to provide an integrated framework for understanding the complex role of oxLDL as a cross-organ biomarker in multisystem neovascular diseases and to offer a theoretical basis for its potential as a therapeutic target.