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Inflammation, oxidative stress and renin angiotensin system in atherosclerosis
Kazim Husain1, Wilfredo Hernandez1, Rais A Ansari1
1Kazim Husain, Leon Ferder, Department of Physiology, Pharmacology and Toxicology, Ponce School of Medicine, Ponce, PR 00732, United States.
Insights
Atherosclerosis, a chronic inflammatory disease, involves endothelial dysfunction driven by risk factors. Targeting the renin-angiotensin system (RAS) and inflammation shows promise in slowing disease progression and improving vascular health.
Area of Science:
- Cardiovascular Science
- Inflammation Biology
- Pharmacology
Background:
- Atherosclerosis is a leading cause of global mortality, characterized by chronic inflammation and endothelial dysfunction.
- Cardiovascular risk factors like diabetes, hypertension, and smoking initiate atherogenesis via oxidative stress and an imbalance in vasodilating/vasoconstricting factors.
- The renin-angiotensin system (RAS), particularly angiotensin II (Ang II), plays a crucial role in endothelial function, inflammation, and plaque stability during atherosclerosis.
Purpose of the Study:
- To review the role of the renin-angiotensin system (RAS) and anti-inflammatory agents in atherosclerosis.
- To explore therapeutic strategies targeting inflammatory pathways and RAS in managing atherosclerotic disease.
- To highlight recent findings on vitamin D analogs in preclinical atherosclerosis models.
Main Methods:
- Literature review of studies on anti-inflammatory agents and RAS inhibitors in atherosclerosis.
- Analysis of clinical trial data demonstrating vascular benefits of these agents.
- Inclusion of preclinical data on vitamin D analogs (paricalcitol) in atherosclerotic mice.
Main Results:
- Anti-inflammatory agents and RAS inhibitors demonstrated vascular benefits and reduced coronary atherosclerosis progression in patients.
- Studies showed decreased vascular inflammatory markers, improved intima-media thickness, and reduced plaque volume in patients with atherosclerosis.
- Preclinical studies indicated therapeutic efficacy of vitamin D analogs, such as paricalcitol, in managing atherosclerosis.
Conclusions:
- Targeting inflammatory processes and the RAS offers a promising therapeutic avenue for slowing atherosclerosis progression.
- Clinical studies support the use of anti-inflammatory agents and RAS inhibitors for vascular benefits in atherosclerotic patients.
- Further research into agents like vitamin D analogs may provide novel treatment strategies for atherosclerosis.
Abstract:
Atherosclerosis is a chronic inflammatory disease associated with cardiovascular dysfunction including myocardial infarction, unstable angina, sudden cardiac death, stroke and peripheral thromboses. It has been predicted that atherosclerosis will be the primary cause of death in the world by 2020. Atherogenesis is initiated by endothelial injury due to oxidative stress associated with cardiovascular risk factors including diabetes mellitus, hypertension, cigarette smoking, dyslipidemia, obesity, and metabolic syndrome. The impairment of the endothelium associated with cardiovascular risk factors creates an imbalance between vasodilating and vasoconstricting factors, in particular, an increase in angiotensin II (Ang II) and a decrease in nitric oxide. The renin-angiotensin system (RAS), and its primary mediator Ang II, also have a direct influence on the progression of the atherosclerotic process via effects on endothelial function, inflammation, fibrinolytic balance, and plaque stability. Anti-inflammatory agents [statins, secretory phospholipase A2 inhibitor, lipoprotein-associated phospholipase A2 inhibitor, 5-lipoxygenase activating protein, chemokine motif ligand-2, C-C chemokine motif receptor 2 pathway inhibitors, methotrexate, IL-1 pathway inhibitor and RAS inhibitors (angiotensin-converting enzyme inhibitors)], Ang II receptor blockers and ranin inhibitors may slow inflammatory processes and disease progression. Several studies in human using anti-inflammatory agents and RAS inhibitors revealed vascular benefits and reduced progression of coronary atherosclerosis in patients with stable angina pectoris; decreased vascular inflammatory markers, improved common carotid intima-media thickness and plaque volume in patients with diagnosed atherosclerosis. Recent preclinical studies have demonstrated therapeutic efficacy of vitamin D analogs paricalcitol in ApoE-deficient atherosclerotic mice.
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