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The effects of pigment epithelium-derived factor on atherosclerosis: putative mechanisms of the process
Shouyuan Ma1, Shuxia Wang2, Man Li1
1Department of Geriatric Cardiology, Chinese PLA General Hospital, Beijing, 100853, China.
Insights
Pigment epithelium-derived factor (PEDF) shows promise in combating atherosclerosis, a major cause of cardiovascular disease (CVD). Research indicates PEDF protects against endothelial dysfunction and inflammation, suggesting its therapeutic potential.
Area of Science:
- Biochemistry
- Cardiology
- Molecular Biology
Background:
- Cardiovascular disease (CVD) remains a leading global cause of mortality, with atherosclerosis as its primary driver.
- Current therapeutic strategies for atherosclerosis are limited, necessitating the development of novel treatments.
- Pigment epithelium-derived factor (PEDF) possesses multifaceted protective properties, including anti-inflammatory and anti-oxidant effects, making it a candidate for atherosclerosis prevention.
Purpose of the Study:
- To review the role of Pigment epithelium-derived factor (PEDF) in the pathogenesis of atherosclerosis.
- To explore the therapeutic potential of PEDF in managing cardiovascular disease (CVD).
- To summarize PEDF's impact on endothelial dysfunction, inflammation, oxidative stress, angiogenesis, and cell proliferation in atherosclerosis.
Main Methods:
- Literature review summarizing existing research on PEDF and atherosclerosis.
- Analysis of studies investigating PEDF's association with acute coronary syndrome (ACS) and coronary artery disease (CAD).
- Examination of molecular mechanisms, including the effects of oxidized-low density lipoprotein (ox-LDL) and D-4F on PEDF levels and endothelial cells, and PEDF's influence on the Wnt/β-catenin pathway.
Main Results:
- PEDF exhibits anti-inflammatory, anti-oxidant, anti-angiogenic, and anti-thrombotic properties beneficial in atherosclerosis.
- PEDF levels are associated with acute coronary syndrome (ACS), and specific PEDF gene polymorphisms correlate with coronary artery disease (CAD).
- Oxidized-low density lipoprotein (ox-LDL) decreases PEDF via reactive oxygen species (ROS), while D-4F preserves PEDF and protects endothelial cells; PEDF may inhibit the Wnt/β-catenin pathway to alleviate endothelial injury.
Conclusions:
- PEDF plays a significant role in mitigating key processes involved in atherosclerosis development.
- PEDF demonstrates potential as a novel therapeutic target for atherosclerosis and related cardiovascular diseases (CVD).
- Further research into PEDF's mechanisms and therapeutic applications is warranted for high-risk patients.
Abstract:
Cardiovascular disease (CVD) is a leading cause of death worldwide. Atherosclerosis is believed to be the major cause of CVD, characterized by atherosclerotic lesion formation and plaque disruption. Although remarkable advances in understanding the mechanisms of atherosclerosis have been made, the application of these theories is still limited in the prevention and treatment of atherosclerosis. Therefore, novel and effective strategies to treat high-risk patients with atherosclerosis require further development. Pigment epithelium-derived factor (PEDF), a glycoprotein with anti-inflammatory, anti-oxidant, anti-angiogenic, anti-thrombotic and anti-tumorigenic properties, is of considerable interest in the prevention of atherosclerosis. Accumulating research has suggested that PEDF exerts beneficial effects on atherosclerotic lesions and CVD patients. Our group, along with colleagues, has demonstrated that PEDF may be associated with acute coronary syndrome (ACS), and that the polymorphisms of rs8075977 of PEDF are correlated with coronary artery disease (CAD). Moreover, we have explored the anti-atherosclerosis mechanisms of PEDF, showing that oxidized-low density lipoprotein (ox-LDL) reduced PEDF concentrations through the upregulation of reactive oxygen species (ROS), and that D-4F can protect endothelial cells against ox-LDL-induced injury by preventing the downregulation of PEDF. Additionally, PEDF might alleviate endothelial injury by inhibiting the Wnt/β-catenin pathway. These data suggest that PEDF may be a novel therapeutic target for the treatment of atherosclerosis. In this review, we will summarize the role of PEDF in the development of atherosclerosis, focusing on endothelial dysfunction, inflammation, oxidative stress, angiogenesis and cell proliferation. We will also discuss its promising therapeutic implications for atherosclerosis.
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