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Dysfunction of Microcirculation in Atherosclerosis: Implications of Nitric Oxide, Oxidative Stress, and Inflammation

Marta Aleksandrowicz1, Marek Konop2, Mateusz Rybka2

  • 1Laboratory of Preclinical Research and Environmental Agents, Mossakowski Medical Research Institute, Polish Academy of Sciences, 5 A. Pawińskiego Street, 02-106 Warsaw, Poland.

International Journal of Molecular Sciences
|July 12, 2025
PubMed

Insights

Atherosclerosis (AS), a major cause of cardiovascular disease (CVD), stems from endothelial dysfunction. Key risk factors like hypertension (HT) and hyperlipidemia (HPL) disrupt nitric oxide (NO) production, driving AS progression.

Area of Science:

  • Cardiovascular Medicine
  • Pathophysiology
  • Vascular Biology

Background:

  • Cardiovascular diseases (CVDs) are the leading global cause of mortality, with atherosclerosis (AS) being a primary underlying pathology.
  • Hypertension (HT), hyperlipidemia (HPL), and hyperglycemia (HG) are significant public health concerns and major risk factors for CVD, often linked to endothelial dysfunction (ED).
  • Endothelial cells are crucial for vascular health, and their dysfunction is central to the initiation and progression of AS.

Purpose of the Study:

  • To synthesize recent advances in understanding the pathophysiology of multifactorial-related atherosclerosis (AS).
  • To explore the role of endothelial dysfunction (ED) and its relationship with key risk factors in AS development.
  • To highlight the importance of nitric oxide (NO) bioavailability in maintaining vascular homeostasis and its disruption in AS.

Main Methods:

  • This review synthesizes current research on the pathophysiology of atherosclerosis.
  • It examines the interplay between risk factors (HT, HPL, HG) and endothelial cell function.
  • The review discusses the role of oxidative stress, inflammation, and nitric oxide (NO) in AS pathogenesis.

Main Results:

  • Endothelial dysfunction (ED) is a critical factor in the development and progression of atherosclerosis (AS).
  • Risk factors such as hypertension (HT), hyperlipidemia (HPL), and hyperglycemia (HG) contribute to ED and AS.
  • Disturbances in nitric oxide (NO) synthesis and bioavailability, exacerbated by oxidative stress and inflammation, are integral to AS development.

Conclusions:

  • Endothelial dysfunction is a central mechanism in multifactorial atherosclerosis.
  • Managing risk factors like HT, HPL, and HG is crucial for preventing AS progression.
  • Restoring nitric oxide (NO) bioavailability may offer therapeutic strategies against AS.

Keywords:
atherosclerosisendothelial dysfunctionhypercholesterolemiahyperglycaemiainflammationmicrocirculationoxidative stress

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