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Emerging role of damage-associated molecular patterns derived from mitochondria in inflammation

(2011) TRENDS IN IMMUNOLOGY. 32(4). p.157-164
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Ghent researchers on unfolded proteins in inflammatory disease (GROUP-ID)
Abstract
Cell death and injury often lead to release or exposure of intracellular molecules called damage-associated molecular patterns (DAMPs) or cell death-associated molecules. These molecules are recognized by the innate immune system by pattern recognition receptors the same receptors that detect pathogen-associated molecular patterns, thus revealing similarities between pathogen-induced and non-infectious inflammatory responses. Many DAMPs are derived from the plasma membrane, nucleus, endoplasmic reticulum and cytosol. Recently, mitochondria have emerged as other organelles that function as a source of DAMPs. Here, we highlight the significance of mitochondria! DAMPs and discuss their contribution to inflammation and development of human pathologies.
Keywords
NECROTIC CELL-DEATH, APOPTOSIS, FIND-ME SIGNAL, CYTOCHROME-C, IN-VIVO, EXTRACELLULAR ATP, OXIDATIVE STRESS, PROTEIN-COUPLED RECEPTORS, INNATE IMMUNE-RESPONSES, FORMYL PEPTIDE RECEPTORS

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Citation

Please use this url to cite or link to this publication:

MLA
Krysko, Dmitri, Patrizia Agostinis, Olga Krysko, et al. “Emerging Role of Damage-associated Molecular Patterns Derived from Mitochondria in Inflammation.” TRENDS IN IMMUNOLOGY 32.4 (2011): 157–164. Print.
APA
Krysko, Dmitri, Agostinis, P., Krysko, O., Garg, A. D., Bachert, C., Lambrecht, B., & Vandenabeele, P. (2011). Emerging role of damage-associated molecular patterns derived from mitochondria in inflammation. TRENDS IN IMMUNOLOGY, 32(4), 157–164.
Chicago author-date
Krysko, Dmitri, Patrizia Agostinis, Olga Krysko, Abhishek D Garg, Claus Bachert, Bart Lambrecht, and Peter Vandenabeele. 2011. “Emerging Role of Damage-associated Molecular Patterns Derived from Mitochondria in Inflammation.” Trends in Immunology 32 (4): 157–164.
Chicago author-date (all authors)
Krysko, Dmitri, Patrizia Agostinis, Olga Krysko, Abhishek D Garg, Claus Bachert, Bart Lambrecht, and Peter Vandenabeele. 2011. “Emerging Role of Damage-associated Molecular Patterns Derived from Mitochondria in Inflammation.” Trends in Immunology 32 (4): 157–164.
Vancouver
1.
Krysko D, Agostinis P, Krysko O, Garg AD, Bachert C, Lambrecht B, et al. Emerging role of damage-associated molecular patterns derived from mitochondria in inflammation. TRENDS IN IMMUNOLOGY. 2011;32(4):157–64.
IEEE
[1]
D. Krysko et al., “Emerging role of damage-associated molecular patterns derived from mitochondria in inflammation,” TRENDS IN IMMUNOLOGY, vol. 32, no. 4, pp. 157–164, 2011.
@article{1224403,
  abstract     = {Cell death and injury often lead to release or exposure of intracellular molecules called damage-associated molecular patterns (DAMPs) or cell death-associated molecules. These molecules are recognized by the innate immune system by pattern recognition receptors the same receptors that detect pathogen-associated molecular patterns, thus revealing similarities between pathogen-induced and non-infectious inflammatory responses. Many DAMPs are derived from the plasma membrane, nucleus, endoplasmic reticulum and cytosol. Recently, mitochondria have emerged as other organelles that function as a source of DAMPs. Here, we highlight the significance of mitochondria! DAMPs and discuss their contribution to inflammation and development of human pathologies.},
  author       = {Krysko, Dmitri and Agostinis, Patrizia and Krysko, Olga and Garg, Abhishek D and Bachert, Claus and Lambrecht, Bart and Vandenabeele, Peter},
  issn         = {1471-4906},
  journal      = {TRENDS IN IMMUNOLOGY},
  keywords     = {NECROTIC CELL-DEATH,APOPTOSIS,FIND-ME SIGNAL,CYTOCHROME-C,IN-VIVO,EXTRACELLULAR ATP,OXIDATIVE STRESS,PROTEIN-COUPLED RECEPTORS,INNATE IMMUNE-RESPONSES,FORMYL PEPTIDE RECEPTORS},
  language     = {eng},
  number       = {4},
  pages        = {157--164},
  title        = {Emerging role of damage-associated molecular patterns derived from mitochondria in inflammation},
  url          = {http://dx.doi.org/10.1016/j.it.2011.01.005},
  volume       = {32},
  year         = {2011},
}

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