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The Role of HSP70 in the Protection of: (A) The Brain in Alzheimer’s Disease and (B) The Heart in Cardiac Surgery

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Part of the book series: SpringerBriefs in Biochemistry and Molecular Biology ((BRIEFSBIOCHEM,volume 6))

Abstract

The accumulation of aggregated, misfolded proteins and the appearance of neurotoxic aggregates of Aβ and tau proteins play a key role in the development of Alzheimer’s disease. HSP70 can inhibit neurodegeneration associated with Alzheimer’s disease because this protein can: (i) aid in the degradation of intracellular and extracellular Aβ aggregates; (ii) restrict tau protein hyperphosphorylation and facilitate the degradation of dysfunctional tau proteins; (iii) limit NO overproduction; and (iv) regulate apoptosis. It is also likely that HSP70 may delay the development of Alzheimer’s disease by limiting insulin receptor desensitization. HSP70 can limit ischemia myocardial injury by: (i) maintaining protein homeostasis in cells; (ii) stabilizing lysosomal membranes; (iii) inhibiting the excessive activation of ADP-ribose polymerase; and (iv) blocking ischemia-induced apoptosis. During the excessive systemic inflammatory response syndrome (SIRS) that occurs in heart surgery, extracellular HSP70 initiates inflammatory effects through the stimulation of immune cell receptors. In contrast, intracellular HSP70, exerts anti-inflammatory effects on the inflammatory balance of SIRS by inhibiting proinflammatory signaling in immune cells.

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Malyshev, I. (2013). The Role of HSP70 in the Protection of: (A) The Brain in Alzheimer’s Disease and (B) The Heart in Cardiac Surgery. In: Immunity, Tumors and Aging: The Role of HSP70. SpringerBriefs in Biochemistry and Molecular Biology, vol 6. Springer, Dordrecht. https://doi.org/10.1007/978-94-007-5943-5_8

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