| Literature DB >> 33711363 |
Manon Callens1, Nina Kraskovskaya2, Kristina Derevtsova2, Wim Annaert3, Geert Bultynck4, Ilya Bezprozvanny5, Tim Vervliet1.
Abstract
The family of B-cell lymphoma-2 (Bcl-2) proteins exerts key functions in cellular health. Bcl-2 primarily acts in mitochondria where it controls the initiation of apoptosis. However, during the last decades, it has become clear that this family of proteins is also involved in controlling intracellular Ca2+ signaling, a critical process for the function of most cell types, including neurons. Several anti- and pro-apoptotic Bcl-2 family members are expressed in neurons and impact neuronal function. Importantly, expression levels of neuronal Bcl-2 proteins are affected by age. In this review, we focus on the emerging roles of Bcl-2 proteins in neuronal cells. Specifically, we discuss how their dysregulation contributes to the onset, development, and progression of neurodegeneration in the context of Alzheimer's disease (AD). Aberrant Ca2+ signaling plays an important role in the pathogenesis of AD, and we propose that dysregulation of the Bcl-2-Ca2+ signaling axis may contribute to the progression of AD and that herein, Bcl-2 may constitute a potential therapeutic target for the treatment of AD.Entities:
Keywords: Alzheimer's disease; Apoptosis; Bcl-2; Calcium; Mitochondria; Neurons
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Year: 2021 PMID: 33711363 PMCID: PMC8041352 DOI: 10.1016/j.bbamcr.2021.118997
Source DB: PubMed Journal: Biochim Biophys Acta Mol Cell Res ISSN: 0167-4889 Impact factor: 4.739