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An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
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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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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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The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
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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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Related Experiment Video

Updated: Oct 7, 2025

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
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Inflammation Resolution: Implications for Atherosclerosis.

Amanda C Doran1

  • 1Department of Medicine, Division of Cardiovascular Medicine, Vanderbilt Institute for Infection, Immunology and Inflammation, Department of Molecular Physiology and Biophysics and Department of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, TN.

Circulation Research
|January 7, 2022
PubMed
Summary
This summary is machine-generated.

Failed resolution of inflammation, crucial for tissue repair, drives chronic diseases like atherosclerosis. Key failures include mediator imbalance, poor dead cell clearance, and altered immune cell function. New regulators offer therapeutic potential.

Keywords:
T-lymphocytes, regulatoryatherosclerosiscardiovascular diseasesinflammationmacrophagesmetabolismphagocytosis

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Area of Science:

  • Immunology
  • Pathophysiology
  • Biomedical Science

Background:

  • Inflammation resolution is a vital, active process to limit tissue damage and initiate repair.
  • Failure of resolution leads to persistent inflammation, a key factor in chronic inflammatory diseases.
  • Atherosclerosis is a chronic inflammatory disease where resolution failure plays a significant role.

Purpose of the Study:

  • To review the primary mechanisms of failed resolution in atherosclerosis.
  • To discuss emerging concepts regulating resolution processes.
  • To highlight the translational significance of understanding resolution failure.

Main Methods:

  • Literature review of inflammatory resolution mechanisms.
  • Analysis of mediator production in atherosclerosis.
  • Examination of immune cell function and efferocytosis in chronic inflammation.
  • Discussion of novel regulatory pathways.

Main Results:

  • Key failures in atherosclerosis resolution include an imbalance of pro-inflammatory to pro-resolving mediators.
  • Impaired clearance of dead cells (efferocytosis) contributes to sustained inflammation.
  • Functional alterations in immune cells promote ongoing inflammatory processes.
  • Emerging concepts suggest new regulatory targets for resolution.

Conclusions:

  • Failed resolution is a central mechanism in the pathogenesis of atherosclerosis.
  • Targeting resolution pathways, including mediator balance and efferocytosis, holds therapeutic promise.
  • Understanding novel regulators is crucial for developing effective treatments for chronic inflammatory diseases.