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Mitochondrial dysfunction and oxidative stress activate inflammasomes: impact on the aging process and age-related diseases 总被引:1,自引:1,他引:0
Salminen A Ojala J Kaarniranta K Kauppinen A 《Cellular and molecular life sciences : CMLS》2012,69(18):2999-3013
Oxidative stress and low-grade inflammation are the hallmarks of the aging process and are even more enhanced in many age-related degenerative diseases. Mitochondrial dysfunction and oxidative stress can provoke and potentiate inflammatory responses, but the mechanism has remained elusive. Recent studies indicate that oxidative stress can induce the assembly of multiprotein inflammatory complexes called the inflammasomes. Nod-like receptor protein 3 (NLRP3) is the major immune sensor for cellular stress signals, e.g., reactive oxygen species, ceramides, and cathepsin B. NLRP3 activation triggers the caspase-1-mediated maturation of the precursors of IL-1β and IL-18 cytokines. During aging, the autophagic clearance of mitochondria declines and dysfunctional mitochondria provoke chronic oxidative stress, which disturbs the cellular redox balance. Moreover, increased NF-κB signaling observed during aging could potentiate the expression of NLRP3 and cytokine proforms enhancing the priming of NLRP3 inflammasomes. Recent studies have demonstrated that NLRP3 activation is associated with several age-related diseases, e.g., the metabolic syndrome. We will review here the emerging field of inflammasomes in the appearance of the proinflammatory phenotype during the aging process and in age-related diseases. 相似文献
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Summary The results showed that the total content of lipids, which could be peroxidized with Fe(2+)/ascorbate stimulation in vitro, was 45.4% and 53.7% higher than normal in the dystrophic hamster muscle at the age of 1 and 3 months, respectively. Correspondingly, the susceptibility to lipid peroxidation (stimulated by ADP-chelated iron at 37°C) was 38.6–74.3% higher in dystrophic muscles. The increases were not related to necrotic lesions and inflammation observed. The activities of glucose-6-phosphate dehydrogenase, glutathione reductase, thioredoxin reductase and catalase were increased in dystrophic muscles but those of superoxide dismutases and glutathione peroxidase were unaffected. 相似文献
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Summary Chronic daily intake of 0.5% H2O2 in drinking water decreased Se-dependent glutathione peroxidase (Se-GSHPx) activity in rat skeletal muscle, kidney and liver. Non-Se GSHPx activity decreased in kidney. Deprivation of drinking water decreased Se-GSHPx activity in kidney and non-Se GSHPx activity in kidney and liver. H2O2 intake decreased activity of catalase in rat skeletal muscle. H2O2 intake or water deprivation caused no changes in these enzyme activities in mice. 相似文献
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Salminen A Ojala J Huuskonen J Kauppinen A Suuronen T Kaarniranta K 《Cellular and molecular life sciences : CMLS》2008,65(7-8):1049-1058
Research on aging in model organisms has revealed different molecular mechanisms involved in the regulation of the lifespan.
Studies on Saccharomyces cerevisiae have highlighted the role of the Sir2 family of genes, human Sirtuin homologs, as the longevity factors. In Caenorhabditis elegans, the daf-16 gene, a mammalian homolog of FoxO genes, was shown to function as a longevity gene. A wide array of studies has
provided evidence for a role of the activation of innate immunity during aging process in mammals. This process has been called
inflamm-aging. The master regulator of innate immunity is the NF-κB system. In this review, we focus on the several interactions
of aging-associated signaling cascades regulated either by Sirtuins and FoxOs or NF-κB signaling pathways. We provide evidence
that signaling via the longevity factors of FoxOs and SIRT1 can inhibit NF-κB signaling and simultaneously protect against inflamm-aging process.
Received 4 October 2007; received after revision 7 November 2007; accepted 9 November 2007 相似文献
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Sam Kaitaniemi Heli Elovaara Kirsi Grön Heidi Kidron Janne Liukkonen Tiina Salminen Marko Salmi Sirpa Jalkanen Kati Elima 《Cellular and molecular life sciences : CMLS》2009,66(16):2743-2757
Semicarbazide-sensitive amine oxidases (SSAOs) catalyze oxidative deamination of primary amines, but the true physiological
function of these enzymes is still poorly understood. Here, we have studied the functional and structural characteristics
of a human cell-surface SSAO, AOC2, which is homologous to the better characterized family member, AOC3. The preferred in
vitro substrates of AOC2 were found to be 2-phenylethylamine, tryptamine and p-tyramine instead of methylamine and benzylamine, the favored substrates of AOC3. Molecular modeling suggested structural
differences between AOC2 and AOC3, which provide AOC2 with the capability to use the larger monoamines as substrates. Even
though AOC2 mRNA was expressed in many tissues, the only tissues with detectable AOC2-like enzyme activity were found in the
eye. Characterization of AOC2 will help in evaluating the contribution of this enzyme to the pathological processes attributed
to the SSAO activity and in designing specific inhibitors for the individual members of the SSAO family.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users. 相似文献
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The permeability of the blood-brain barrier to sodium fluorescein, or fluorescein-labelled dextrans of various molecular weights, was investigated. Unlike the capillaries in both the area postrema and the eminentia mediana, the capillaries of the cerebral cortex were impermeable to all the intravenous tracer substances used. 相似文献
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Apoptosis is a vital component in the evolutionarily conserved host defense system. Apoptosis is the guardian of tissue integrity
by removing unfit and injured cells without evoking inflammation. However, apoptosis seems to be a double-edged sword since
during low-level chronic stress, such as in aging, increased resistance to apoptosis can lead to the survival of functionally
deficient, post-mitotic cells with damaged housekeeping functions. Senescent cells are remarkably resistant to apoptosis,
and several studies indicate that host defense mechanisms can enhance anti-apoptotic signaling, which subsequently induces
a senescent, pro-inflammatory phenotype during the aging process. At the molecular level, age-related resistance to apoptosis
involves (1) functional deficiency in p53 network, (2) increased activity in the NF-κB-IAP/JNK axis, and (3) changes in molecular
chaperones, microRNAs, and epigenetic regulation. We will discuss the molecular basis of age-related resistance to apoptosis
and emphasize that increased resistance could enhance the aging process. 相似文献