6533b86efe1ef96bd12cc96b
RESEARCH PRODUCT
Hsp60 and human aging: Les liaisons dangereuses
Alberto J.l. MacarioFelicia FarinaGiuseppe BonaventuraMarino Gammazza AAnna M. CzarneckaGiovanni ZummoFrancesco CappelloConway De Macario EFrancesco Carinisubject
SenescenceAginganimal structuresOsteoporosischemical and pharmacologic phenomenaInflammationDiseaseBiologycomplex mixturesMitochondrial ProteinsPathogenesisImmune systemDiabetes mellitusmedicineHumansCellular SenescenceAutoantibodiesHeart FailurefungiHSP 60 AGING CHAPERONES.Neurodegenerative DiseasesChaperonin 60Atherosclerosismedicine.diseaseMitochondriaImmune SystemImmunologyHSP60Arthropathy Neurogenicmedicine.symptomdescription
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.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2013-01-02 | Frontiers in Bioscience |