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Related Concept Videos

Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

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Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
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Inflammation: Introduction01:28

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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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Inflammatory Response01:28

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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.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
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Inflammation01:38

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Overview
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Acute Inflammation I: Cellular Phase01:26

Acute Inflammation I: Cellular Phase

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The cellular phase of acute inflammation is a tightly orchestrated sequence of events that recruits leukocytes, primarily neutrophils, to sites of tissue injury or infection. Following the initial vascular changes, this phase ensures effective immune cell migration, activation, and function at the affected site to eliminate pathogens and initiate tissue repair.Leukocyte Recruitment CascadeLeukocyte recruitment happens in four steps: margination, adhesion, transmigration, and chemotaxis. Reduced...
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Acute Inflammation II: Local and Systemic Effects01:25

Acute Inflammation II: Local and Systemic Effects

56
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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Related Experiment Video

Updated: May 2, 2026

Cellular Membrane Affinity Chromatography Columns to Identify Specialized Plant Metabolites Interacting with Immobilized Tropomyosin Kinase Receptor B
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Inflammaging: From Mechanisms to Clinical Implications and Targeted Interventions.

Rola S Zeidan1,2, Aditya S Shirali3, Simon Reinhard2

  • 1Department of Physiology and Aging, College of Medicine, University of Florida, Gainesville, Florida, USA.

Aging and Disease
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Inflammaging, a chronic inflammatory state linked to aging, drives functional decline and age-associated diseases. Understanding its multifaceted origins and impact is key to developing interventions for extended health-span.

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Area of Science:

  • Gerontology and Immunology
  • Molecular Biology
  • Biomedical Science

Background:

  • Inflammaging is a chronic, low-grade inflammatory state associated with biological aging.
  • It contributes to functional decline, frailty, and age-associated diseases by promoting tissue damage and metabolic dysregulation.
  • Key features include elevated damage-associated molecular patterns (DAMPs), pro-inflammatory cytokines, and senescent cells with a senescence-associated secretory phenotype (SASP).

Purpose of the Study:

  • To distinguish inflammaging from general chronic inflammation.
  • To synthesize current understanding of inflammaging's biological origins and mechanistic drivers.
  • To examine the role of inflammaging in clinical outcomes such as sarcopenia, neurodegeneration, and cardiovascular disease.

Main Methods:

  • Review and synthesis of existing literature on inflammaging.
  • Analysis of biological mechanisms, including DAMPs, cytokines, cellular senescence, and metabolic imbalance.
  • Examination of clinical outcomes and potential translational frameworks.

Main Results:

  • Inflammaging impairs immune surveillance, increases oxidative stress, and enhances tissue vulnerability.
  • It is influenced by chronological aging, behavioral, environmental, psychosocial, and genetic factors, indicating a modifiable nature.
  • Evidence links inflammaging to sarcopenia, neurodegeneration, and cardiovascular disease progression.

Conclusions:

  • Inflammaging is a critical component of aging, impacting health-span and disease risk.
  • A conceptual framework is proposed linking inflammaging mechanisms to biomarkers, AI risk stratification, and precision interventions.
  • Further research and multi-dimensional strategies are needed to promote resilience and extend health-span by targeting inflammaging.