Redox-dependent calpain signaling in airway and pulmonary vascular remodeling in COPD

Research output: Chapter in Book/Report/Conference proceedingChapter

2 Citations (Scopus)

Abstract

The calcium-dependent cytosolic, neutral, thiol endopeptidases, calpains, perform limited cleavage of their substrates thereby irreversibly changing their functions. Calpains have been shown to be involved in several physiological processes such as cell motility, proliferation, cell cycle, signal transduction, and apoptosis. Overactivation of calpain or mutations in the calpain genes contribute to a number of pathological conditions including neurodegenerative disorders, rheumatoid arthritis, cancer, and lung diseases. High concentrations of reactive oxygen and nitrogen species (RONS) originated from cigarette smoke or released by numerous cell types such as activated inflammatory cells and other respiratory cells cause oxidative and nitrosative stress contributing to the pathogenesis of COPD. RONS and calpain play important roles in the development of airway and pulmonary vascular remodeling in COPD. Published data show that increased RONS production is associated with increased calpain activation and/or elevated calpain protein level, leading to epithelial or endothelial barrier dysfunction, neovascularization, lung inflammation, increased smooth muscle cell proliferation, and deposition of extracellular matrix protein. Further investigation of the redox-dependent calpain signaling may provide future targets for the prevention and treatment of COPD.

Original languageEnglish (US)
Title of host publicationAdvances in Experimental Medicine and Biology
PublisherSpringer New York LLC
Pages139-160
Number of pages22
Volume967
DOIs
StatePublished - 2017

Publication series

NameAdvances in Experimental Medicine and Biology
Volume967
ISSN (Print)0065-2598
ISSN (Electronic)2214-8019

Fingerprint

Calpain
Chronic Obstructive Pulmonary Disease
Oxidation-Reduction
Lung
Reactive Nitrogen Species
Reactive Oxygen Species
Cell proliferation
Cell Proliferation
Physiological Phenomena
Neprilysin
Endopeptidases
Signal transduction
Pulmonary diseases
Vascular Remodeling
Extracellular Matrix Proteins
Sulfhydryl Compounds
Smoke
Tobacco Products
Neurodegenerative Diseases
Lung Diseases

Keywords

  • Calpain
  • Cigarette smoke
  • COPD
  • Reactive oxygen and nitrogen species
  • Remodeling

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Kovacs, L., & Su, Y. (2017). Redox-dependent calpain signaling in airway and pulmonary vascular remodeling in COPD. In Advances in Experimental Medicine and Biology (Vol. 967, pp. 139-160). (Advances in Experimental Medicine and Biology; Vol. 967). Springer New York LLC. https://doi.org/10.1007/978-3-319-63245-2_9

Redox-dependent calpain signaling in airway and pulmonary vascular remodeling in COPD. / Kovacs, Laszlo; Su, Yunchao.

Advances in Experimental Medicine and Biology. Vol. 967 Springer New York LLC, 2017. p. 139-160 (Advances in Experimental Medicine and Biology; Vol. 967).

Research output: Chapter in Book/Report/Conference proceedingChapter

Kovacs, L & Su, Y 2017, Redox-dependent calpain signaling in airway and pulmonary vascular remodeling in COPD. in Advances in Experimental Medicine and Biology. vol. 967, Advances in Experimental Medicine and Biology, vol. 967, Springer New York LLC, pp. 139-160. https://doi.org/10.1007/978-3-319-63245-2_9
Kovacs L, Su Y. Redox-dependent calpain signaling in airway and pulmonary vascular remodeling in COPD. In Advances in Experimental Medicine and Biology. Vol. 967. Springer New York LLC. 2017. p. 139-160. (Advances in Experimental Medicine and Biology). https://doi.org/10.1007/978-3-319-63245-2_9
Kovacs, Laszlo ; Su, Yunchao. / Redox-dependent calpain signaling in airway and pulmonary vascular remodeling in COPD. Advances in Experimental Medicine and Biology. Vol. 967 Springer New York LLC, 2017. pp. 139-160 (Advances in Experimental Medicine and Biology).
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