Literature DB >> 15345150

Redox regulation in neurodegeneration and longevity: role of the heme oxygenase and HSP70 systems in brain stress tolerance.

Vittorio Calabrese1, A M Giuffrida Stella, D Allan Butterfield, Giovanni Scapagnini.   

Abstract

Efficient functioning of maintenance and repair processes seems to be crucial for both survival and physical quality of life. This is accomplished by a complex network of the so-called longevity assurance processes, which are composed of several genes termed "vitagenes," among these, the heat shock system, a highly conserved mechanism responsible for the preservation and repair of cellular macromolecules, such as proteins, RNAs, and DNA. Recent studies have shown that the heat shock response contributes to establishing a cytoprotective state in a wide variety of human diseases, including ischemia and reperfusion damage, inflammation, cancer, as well as metabolic and neurodegenerative disorders. Recently, the involvement of the heme oxygenase (HO) pathway in antidegenerative mechanisms has received considerable attention, as it has been demonstrated that the expression of HO is closely related to that of amyloid precursor protein. HO induction occurs together with the induction of other heat shock proteins during various physiopathological conditions. The vasoactive molecule carbon monoxide and the potent antioxidant bilirubin, products of HO-catalyzed reaction, represent a protective system potentially active against brain oxidative injury. Given the broad cytoprotective properties of the heat shock response, molecules inducing this defense mechanism appear to be possible candidates for novel cytoprotective strategies. Particularly, manipulation of endogenous cellular defense mechanisms, via the heat shock response, through nutritional antioxidants or pharmacological compounds, may represent an innovative approach to therapeutic intervention in diseases causing tissue damage, such as neurodegeneration. Consistently, by maintaining or recovering the activity of vitagenes, it is feasible to delay the aging process and decrease the occurrence of age-related diseases with resulting prolongation of a healthy life span.

Entities:  

Mesh:

Substances:

Year:  2004        PMID: 15345150     DOI: 10.1089/ars.2004.6.895

Source DB:  PubMed          Journal:  Antioxid Redox Signal        ISSN: 1523-0864            Impact factor:   8.401


  26 in total

1.  Carbon monoxide promotes VEGF expression by increasing HIF-1alpha protein level via two distinct mechanisms, translational activation and stabilization of HIF-1alpha protein.

Authors:  Yoon Kyung Choi; Chun-Ki Kim; Hansoo Lee; Dooil Jeoung; Kwon-Soo Ha; Young-Guen Kwon; Kyu-Won Kim; Young-Myeong Kim
Journal:  J Biol Chem       Date:  2010-08-19       Impact factor: 5.157

2.  Protective effect of carnosine during nitrosative stress in astroglial cell cultures.

Authors:  V Calabrese; C Colombrita; E Guagliano; M Sapienza; A Ravagna; V Cardile; G Scapagnini; A M Santoro; A Mangiameli; D A Butterfield; A M Giuffrida Stella; E Rizzarelli
Journal:  Neurochem Res       Date:  2005 Jun-Jul       Impact factor: 3.996

3.  Protective effect of exogenous 70-kDa heat shock protein during endotoxic shock (sepsis).

Authors:  G A Kustanova; A N Murashev; I V Guzhova; B A Margulis; I R Prokhorenko; S V Grachev; M B Evgen'ev
Journal:  Dokl Biol Sci       Date:  2006 Nov-Dec

Review 4.  Intersection between metabolic dysfunction, high fat diet consumption, and brain aging.

Authors:  Romina M Uranga; Annadora J Bruce-Keller; Christopher D Morrison; Sun Ok Fernandez-Kim; Philip J Ebenezer; Le Zhang; Kalavathi Dasuri; Jeffrey N Keller
Journal:  J Neurochem       Date:  2010-05-06       Impact factor: 5.372

Review 5.  Interactions of multiple gas-transducing systems: hallmarks and uncertainties of CO, NO, and H2S gas biology.

Authors:  Mayumi Kajimura; Ryo Fukuda; Ryon M Bateman; Takehiro Yamamoto; Makoto Suematsu
Journal:  Antioxid Redox Signal       Date:  2010-07-15       Impact factor: 8.401

6.  Critical Role of Endoplasmic Reticulum Stress in Chronic Intermittent Hypoxia-Induced Deficits in Synaptic Plasticity and Long-Term Memory.

Authors:  Lin-Hao Xu; Hui Xie; Zhi-Hui Shi; Li-Da Du; Yun-Kwok Wing; Albert M Li; Ya Ke; Wing-Ho Yung
Journal:  Antioxid Redox Signal       Date:  2015-05-08       Impact factor: 8.401

7.  Methamphetamine preconditioning causes differential changes in striatal transcriptional responses to large doses of the drug.

Authors:  Jean Lud Cadet; Christie Brannock; Bruce Ladenheim; Michael T McCoy; Genevieve Beauvais; Amber B Hodges; Elin Lehrmann; William H Wood; Kevin G Becker; Irina N Krasnova
Journal:  Dose Response       Date:  2010-07-02       Impact factor: 2.658

Review 8.  Cellular stress responses, the hormesis paradigm, and vitagenes: novel targets for therapeutic intervention in neurodegenerative disorders.

Authors:  Vittorio Calabrese; Carolin Cornelius; Albena T Dinkova-Kostova; Edward J Calabrese; Mark P Mattson
Journal:  Antioxid Redox Signal       Date:  2010-08-28       Impact factor: 8.401

9.  Methamphetamine induces dopamine D1 receptor-dependent endoplasmic reticulum stress-related molecular events in the rat striatum.

Authors:  Subramaniam Jayanthi; Michael T McCoy; Genevieve Beauvais; Bruce Ladenheim; Kristi Gilmore; William Wood; Kevin Becker; Jean Lud Cadet
Journal:  PLoS One       Date:  2009-06-30       Impact factor: 3.240

10.  Methamphetamine preconditioning alters midbrain transcriptional responses to methamphetamine-induced injury in the rat striatum.

Authors:  Jean Lud Cadet; Michael T McCoy; Ning Sheng Cai; Irina N Krasnova; Bruce Ladenheim; Genevieve Beauvais; Natascha Wilson; William Wood; Kevin G Becker; Amber B Hodges
Journal:  PLoS One       Date:  2009-11-12       Impact factor: 3.240

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.