Amadou K.S. Camara, Yi Fan Zhou, Po Chao Wen, Emad Tajkhorshid, and Wai Meng
Kwok.
Mitochondrial VDAC1: A key gatekeeper as potential therapeutic
target.
Frontiers in Physiology, 8:640, 2017.
(PMC: PMC5491678)
CAMA2017-ET
Mitochondria are the key source of ATP that fuels cellular functions, and
they are also central in cellular signaling, cell division and apoptosis.
Dysfunction of mitochondria has been implicated in a wide range of
diseases, including neurodegenerative and cardiac diseases, and various
types of cancer. One of the key proteins that regulate mitochondrial
function is the voltage-dependent anion channel 1 (VDAC1), the most
abundant protein on the outer membrane of mitochondria. VDAC1 is the
gatekeeper for the passages of metabolites, nucleotides, and ions; it plays
a crucial role in regulating apoptosis due to its interaction with apoptotic
and anti-apoptotic proteins, namely members of the Bcl-2 family of
proteins and hexokinase. Therefore, regulation of VDAC1 is crucial not only
for metabolic functions of mitochondria, but also for cell survival. In fact,
multiple lines of evidence have confirmed the involvement of VDAC1 in
several diseases. Consequently, modulation or dysregulation of VDAC1
function can potentially attenuate or exacerbate pathophysiological
conditions. Understanding the role of VDAC1 in health and disease could
lead to selective protection of cells in different tissues and diverse
diseases. The purpose of this review is to discuss the role of VDAC1 in the
pathogenesis of diseases and as a potentially effective target for
therapeutic management of various pathologies.
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