Mitochondrial damage-associated molecular patterns and vascular function

Camilla Ferreira Wenceslau1, Cameron G McCarthy, Theodora Szasz

  • 1Department of Physiology, Georgia Regents University, 1120 15th Street, Augusta, GA 30912, USA.

European Heart Journal
|February 27, 2014
PubMed

Insights

Endogenous molecules, known as damage-associated molecular patterns (DAMPs), alarm the immune system upon cell injury. Mitochondrial DAMPs (mtDAMPs) are potent activators linked to vascular dysfunction and cardiovascular disease.

Area of Science:

  • Immunology
  • Cardiovascular Science
  • Cell Biology

Background:

  • Immune system activation can be triggered by endogenous molecules released during cell death or injury, not just foreign stimuli.
  • These endogenous molecules are collectively termed damage-associated molecular patterns (DAMPs).
  • Mitochondria, due to their bacterial ancestry, release potent immunological activators known as mitochondrial DAMPs (mtDAMPs).

Purpose of the Study:

  • To review recent evidence linking mitochondrial DAMPs (mtDAMPs) and immune system activation.
  • To explore the role of mtDAMPs in vascular dysfunction and cardiovascular disease.
  • To elucidate the mechanisms by which mtDAMPs induce vascular changes following cell death.

Main Methods:

  • Review of recently published scientific literature.
  • Analysis of studies investigating immune system activation by endogenous molecules.
  • Examination of research on mitochondrial DAMPs and their interaction with pattern recognition receptors.
  • Focus on evidence connecting mtDAMPs to cardiovascular system changes.

Main Results:

  • Mitochondrial DAMPs (mtDAMPs) are potent immune activators recognized by innate immune receptors.
  • Some pattern recognition receptors for mtDAMPs are present in the cardiovascular system.
  • Cell death releases mtDAMPs that can induce vascular changes, contributing to disease.

Conclusions:

  • Mitochondrial DAMPs play a significant role in immune system activation.
  • The release of mtDAMPs following cell death is implicated in vascular dysfunction.
  • Further research is needed to fully understand the mechanisms linking mtDAMPs to cardiovascular disease.

Related Concept Videos

Mitochondrial Membranes01:45

Mitochondrial Membranes

A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
11.7K
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
11.9K
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

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...
1.1K
Cellular Injury I: Introduction01:00

Cellular Injury I: Introduction

Cellular injury occurs when a cell cannot maintain homeostasis or adapt to stressors such as hypoxia, toxins, or trauma. Depending on severity and duration, injury may be reversible, allowing recovery, or irreversible, leading to cell death.General Mechanisms of Cell InjuryAlthough causes vary, most cellular injuries arise from a few key mechanisms that disrupt essential functions and often amplify one another. Cell survival depends on the extent and balance of these disturbances.ATP depletion...
68
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
63
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
54