Related Experiment Video

Updated: Jul 31, 2026

In vivo Imaging Method to Distinguish Acute and Chronic Inflammation
07:10

In vivo Imaging Method to Distinguish Acute and Chronic Inflammation

Published on: August 16, 2013

15-Lipoxygenase in glomerular inflammation

A Montero1, K F Badr

  • 1Center for Glomerulonephritis, Renal Division, Emory University, Decatur, GA 30033, USA. amonter@emory.edu

Experimental Nephrology
|January 25, 2000
PubMed

Insights

Glomerulonephritis contributes to end-stage renal disease. This review explores 15-lipoxygenase activation in early glomerular injury and proposes clinical strategies based on new pathophysiological insights.

Area of Science:

  • Nephrology
  • Immunology
  • Molecular Biology

Background:

  • Glomerulonephritis is a leading cause of end-stage renal disease.
  • Understanding early injury mechanisms is crucial for developing novel therapies.
  • Targeting specific pathways offers a promising approach to halt glomerular damage.

Purpose of the Study:

  • To investigate the role of 15-lipoxygenase (15-LO) activation in early, prefibrotic glomerular immune injury.
  • To examine the effects of cytokines released during these inflammatory processes.
  • To propose a clinical strategy for glomerulonephritis based on emerging pathophysiological concepts.

Main Methods:

  • Review of experimental results characterizing 15-lipoxygenase activation.
  • Analysis of cytokine profiles in glomerular immune injury.
  • Evaluation of aspirin's effect on 15-R-HETE synthesis.

Main Results:

  • 15-lipoxygenase activation is implicated in the early stages of glomerular immune injury.
  • Cytokines play a significant role in mediating inflammatory processes.
  • Aspirin influences the synthesis of 15-R-HETE.

Conclusions:

  • 15-lipoxygenase activation is a key mechanism in early glomerulonephritis.
  • Targeted therapies addressing these mechanisms may prevent disease progression.
  • Emerging concepts in glomerulonephritis pathophysiology can guide clinical management.

More Related Videos

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury14:48

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury

Published on: March 21, 2021

Using 2-Photon Microscopy to Quantify the Effects of Chronic Unilateral Ureteral Obstruction on Glomerular Processes11:47

Using 2-Photon Microscopy to Quantify the Effects of Chronic Unilateral Ureteral Obstruction on Glomerular Processes

Published on: March 4, 2022

Related Concept Videos

Acute Inflammation I: Inflammatory Response01:26

Acute Inflammation I: Inflammatory Response

Acute inflammation is a rapid, short-lived physiological response to tissue injury or infection, designed to eliminate harmful agents and initiate repair. This tightly regulated process typically lasts from minutes to several days and is triggered by factors such as microbial invasion, physical trauma, or chemical injury.Recognition and Mediator ReleaseThe inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect damage-associated...
Acute Inflammation II: Cellular Phase01:26

Acute Inflammation II: Cellular Phase

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...
Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

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...
Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

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...