title: Hsp60 and human aging: Les liaisons dangereuses.
abstract: Stressors can cause abnormal intracellular accumulation of Hsp60 and its localization in extramitochondrial sites, secretion, and circulation, with immune system activation. Dysfunction of chaperones associated with their quantitative and qualitative decline with aging (chaperonopathies of aging) characterizes senescence and is a potential causal factor in the physiological deterioration that occurs with it. The role of Hsp60 in aging is not easy to elucidate, because aging is accompanied by pathologies (e.g., cardiovascular and neurodegenerative disorders, osteoporosis, diabetes, cancer, etc.) in which Hsp60 has been implicated but, although those disorders are more frequent in the elderly, they are not unique to them. Therefore, it is difficult to determine what is due to aging and what to an associated disease that can occur regardless of age. Does Hsp60 contribute to the pathogenesis? How and when does Hsp60 interact with the immune system and, thus, contributes to the initiation-progression of the generalized chronic inflammation characteristic of aging? These and related issues are discussed here in the light of reports showing the participation of Hsp60 in aging-associated disorders.
authors.affiliation: Department of Experimental Biomedicine and Clinical Neurosciences, Human Anatomy Section, Emerico Luna, Via del Vespro 129, 90127 Palermo, Italy. francapp@hotmail.com
authors.forename: Francesco
authors.initials: F
authors.lastname: Cappello
authors.forename: Everly
authors.initials: E
authors.lastname: Conway de Macario
authors.forename: Antonella
authors.initials: A
authors.lastname: Marino Gammazza
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Bonaventura
authors.forename: Francesco
authors.initials: F
authors.lastname: Carini
authors.forename: Anna M
authors.initials: AM
authors.lastname: Czarnecka
authors.forename: Felicia
authors.initials: F
authors.lastname: Farina
authors.forename: Giovanni
authors.initials: G
authors.lastname: Zummo
authors.forename: Alberto J L
authors.initials: AJ
authors.lastname: Macario
mesh_terms: D000375:Aging / Q000502:physiology; D001177:Arthropathy, Neurogenic / Q000503:physiopathology; D050197:Atherosclerosis / Q000503:physiopathology; D001323:Autoantibodies / Q000502:physiology; D016922:Cellular Senescence / Q000502:physiology; D018834:Chaperonin 60 / Q000737:chemistry / Q000276:immunology / Q000502:physiology*; D006333:Heart Failure / Q000503:physiopathology; D006801:Humans; D007107:Immune System / Q000502:physiology; D008928:Mitochondria / Q000502:physiology; D024101:Mitochondrial Proteins / Q000737:chemistry / Q000276:immunology / Q000502:physiology*; D019636:Neurodegenerative Diseases / Q000503:physiopathology
chemical_list: D001323:Autoantibodies; D018834:Chaperonin 60; C060293:HSPD1 protein, human; D024101:Mitochondrial Proteins