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Updated: May 8, 2026

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
05:51

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

Published on: May 6, 2014

[Chronic inflammation and atherosclerosis].

P von Hundelshausen1, C Weber

  • 1Institut für Prophylaxe und Epidemiologie der Kreislaufkrankheiten (IPEK), Klinikum der Universität München, Ludwig-Maximilians-Universität München und Deutsches Zentrum für Herz-Kreislaufforschung (DZHK), Partnerstandort Munich Heart Alliance.

Deutsche Medizinische Wochenschrift (1946)
|September 6, 2013
PubMed
Summary
This summary is machine-generated.

Chronic inflammatory diseases share mechanisms with acute inflammation, involving cytokines like IL-1 and TNF-α. Therapies targeting these, such as cytokine antagonists and statins, show promise for rheumatic diseases and cardiovascular health.

More Related Videos

A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites
09:52

A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites

Published on: August 8, 2014

Related Experiment Videos

Last Updated: May 8, 2026

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
05:51

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

Published on: May 6, 2014

A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites
09:52

A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites

Published on: August 8, 2014

Area of Science:

  • Immunology
  • Pathophysiology
  • Pharmacology

Context:

  • Chronic inflammatory diseases (e.g., rheumatic diseases, viral infections, atherosclerosis) share mechanistic similarities and differences with acute inflammation.
  • Key inflammatory mediators include cytokines such as Interleukin-1 (IL-1) and Tumor Necrosis Factor-alpha (TNF-α), which activate endothelium and influence lymphocyte balance.
  • Distinct lymphocyte subpopulations (TH1, TH17, Treg, TH2) play pro- or anti-inflammatory roles through secreted mediators like interferons, interleukins, and chemokines.

Purpose:

  • To explore the mechanistic details of chronic inflammatory disease pathogenesis.
  • To highlight the roles of cytokines and lymphocyte subpopulations in inflammation.
  • To review current and potential therapeutic strategies targeting inflammatory pathways.

Summary:

  • Understanding inflammation's mechanistic details reveals similarities and differences between acute and chronic conditions.
  • Cytokines (IL-1, TNF-α) and specific lymphocyte subtypes (TH1, TH17, Treg, TH2) are central to inflammatory cascades.
  • Interleukin-1 and TNF antagonists are established treatments for rheumatic diseases and are investigated for cardiovascular prevention. Statins' effects on rheumatoid arthritis are also under study.

Impact:

  • IL-1 and TNF antagonists offer therapeutic benefits for rheumatic diseases and show potential in cardiovascular prevention.
  • Investigating the pleiotropic effects of statins may reveal new treatment avenues for rheumatoid arthritis.
  • This research deepens the understanding of inflammatory processes, paving the way for novel therapeutic interventions.