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Related Concept Videos

Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

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Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
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Inflammation01:38

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Coronary Artery Disease II: Pathophysiology01:26

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Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
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Atherosclerosis III: Management01:26

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Management of atherosclerosis involves an integrated strategy encompassing pharmacological treatment, surgical interventions, lifestyle changes, and nutrition therapy to address the multifactorial nature of the disease.Pharmacological TherapyA cornerstone of atherosclerosis management is the use of pharmacological agents. Statins, such as atorvastatin, are pivotal in inhibiting HMG-CoA reductase, an enzyme that catalyzes an initial step in cholesterol synthesis in the liver. This reduction in...
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Coronary Artery Disease I: Introduction01:30

Coronary Artery Disease I: Introduction

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Coronary Artery Disease (CAD): An Overview with Scientific InsightsCoronary Artery Disease (CAD), often referred to as C-A-D, is a prevalent blood vessel disorder classified under the broader category of atherosclerosis. Atherosclerosis is a pathological process characterized by the hardening and narrowing of arteries due to the accumulation of atherosclerotic plaques. These plaques are composed of cholesterol, fatty substances, inflammatory cells, calcium, and fibrin, reducing blood flow to...
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Ischemic Heart Disease: Overview01:17

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Ischemic heart disease occurs when the heart's blood supply dwindles, causing an ominous lack of oxygen and nutrients. This deficiency, stemming from reduced or obstructed blood flow, spells danger, leading to heart muscle damage and dysfunction.
Atherosclerosis, the primary malefactor, orchestrates this dangerous condition. It manifests as the accumulation of fatty deposits, akin to insidious plaques, within arterial walls. As time elapses, these plaques metamorphose, hardening and...
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Related Experiment Video

Updated: Jul 24, 2025

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
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Indoxyl sulfate in atherosclerosis.

Cong Lu1, Li Wu1, Mu-Yao Tang1

  • 1Research Laboratory of Translational Medicine, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, People's Republic of China; Departments of Clinical Medicine, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, People's Republic of China.

Toxicology Letters
|July 6, 2023
PubMed
Summary

Indoxyl sulfate (IS), a uremia toxin, significantly contributes to atherosclerosis (AS) development by promoting vascular dysfunction, inflammation, and oxidative stress. Understanding IS-mediated mechanisms may reveal new therapeutic targets for cardiovascular disease in patients with kidney dysfunction.

Keywords:
AtherosclerosisCalcificationIndoxyl sulfateInflammationThrombosis

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Area of Science:

  • Cardiovascular Research
  • Nephrology
  • Vascular Biology

Background:

  • Atherosclerosis (AS) is a progressive vascular inflammatory disease with complex pathogenesis.
  • Uremic toxins, particularly indoxyl sulfate (IS), are increasingly implicated in cardiovascular complications.
  • The precise molecular mechanisms linking IS to AS remain incompletely understood.

Purpose of the Study:

  • To review the atherogenic effects of indoxyl sulfate (IS).
  • To elucidate the underlying molecular mechanisms of IS-induced AS.
  • To highlight key pathological events in IS-mediated atherosclerosis.

Main Methods:

  • Literature review focusing on indoxyl sulfate and atherosclerosis.
  • Analysis of studies investigating IS's role in vascular endothelium dysfunction, oxidative stress, inflammation, calcification, and thrombosis.
  • Synthesis of evidence on IS's contribution to foam cell formation and arterial medial lesions.

Main Results:

  • Indoxyl sulfate (IS) exhibits multiple atherogenic effects, contributing to vascular endothelium dysfunction.
  • IS promotes vascular oxidative stress, inflammation, calcification, and thrombosis.
  • IS is implicated in arterial medial lesions and foam cell formation, key events in AS development.

Conclusions:

  • Indoxyl sulfate (IS) is a significant contributor to atherosclerosis (AS) development and progression.
  • Targeting IS-mediated pathways could offer novel therapeutic strategies for cardiovascular disease in renal dysfunction patients.
  • Further research into IS-specific signaling is crucial for identifying new therapeutic targets.