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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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Peripheral artery disease (PAD) predominantly results from atherosclerosis, which involves the accumulation of fatty deposits, or plaques, within the walls of arteries. This causes them to narrow and harden, significantly reducing blood flow. PAD predominantly affects the legs, particularly the arteries supplying the thighs and calves. In rare cases, it may involve other arteries, including those in the arms.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty...
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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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Inflammation is a fundamental, protective biological response of vascularized tissues to cellular injury, infection, or harmful stimuli. Its primary function is to eliminate the initial cause of injury, clear necrotic cells and damaged tissue, and initiate the necessary repair processes.Cardinal SignsAcute inflammation presents with classic signs. Redness results from vasodilation and increased blood flow. Heat is due to increased metabolism and circulation. Swelling results from the...
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Acute Inflammation II: Local and Systemic Effects01:25

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Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
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Proinflammation: the key to arterial aging.

Mingyi Wang1, Liqun Jiang1, Robert E Monticone1

  • 1Laboratory of Cardiovascular Science, National Institution on Aging, National Institutes of Health, Biomedical Research Center (BRC), 251 Bayview Boulevard, Baltimore, MD 21224, USA.

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Arterial aging, driven by chronic inflammation, contributes to cardiovascular disease. Suppressing this inflammation may help delay age-related arterial issues.

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Area of Science:

  • Cardiovascular Science
  • Aging Research
  • Inflammation Biology

Background:

  • Arterial aging is a primary driver of cardiovascular disease (CVD) incidence and prevalence.
  • Chronic, low-grade arterial inflammation, often sterile, underlies age-associated arterial remodeling.
  • The angiotensin II cascade significantly contributes to inflammatory signaling in aging arteries.

Purpose of the Study:

  • To elucidate the molecular mechanisms linking arterial aging and cardiovascular disease.
  • To explore the role of chronic inflammation in age-associated arterial structural and functional changes.
  • To investigate the potential for interventions targeting arterial inflammation to mitigate CVD.

Main Methods:

  • Analysis of molecular pathways involved in arterial aging.
  • Characterization of age-associated changes in arterial structure and function.
  • Review of existing literature on inflammation and vascular aging.

Main Results:

  • Aged arteries exhibit endothelial disruption, vascular smooth muscle cell (VMSC) migration and proliferation, extracellular matrix (ECM) deposition, elastin fracture, and matrix calcification/amyloidosis/glycation.
  • Molecular mechanisms of arterial aging are implicated in hypertension and atherosclerosis.
  • Age-associated arterial proinflammation is modifiable.

Conclusions:

  • Chronic arterial inflammation is a key factor in age-related cardiovascular disease.
  • Understanding these inflammatory mechanisms offers therapeutic targets for age-associated arterial diseases.
  • Interventions aimed at suppressing arterial inflammation may delay or ameliorate cardiovascular disease progression.