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2016 ; 48
(2
): 153-68
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Sphingolipids and mitochondrial apoptosis
#MMPMID25620271
Patwardhan GA
; Beverly LJ
; Siskind LJ
J Bioenerg Biomembr
2016[Apr]; 48
(2
): 153-68
PMID25620271
show ga
The sphingolipid family of lipids modulate several cellular processes, including
proliferation, cell cycle regulation, inflammatory signaling pathways, and cell
death. Several members of the sphingolipid pathway have opposing functions and
thus imbalances in sphingolipid metabolism result in deregulated cellular
processes, which cause or contribute to diseases and disorders in humans. A key
cellular process regulated by sphingolipids is apoptosis, or programmed cell
death. Sphingolipids play an important role in both extrinsic and intrinsic
apoptotic pathways depending on the stimuli, cell type and cellular response to
the stress. During mitochondrial-mediated apoptosis, multiple pathways converge
on mitochondria and induce mitochondrial outer membrane permeabilization (MOMP).
MOMP results in the release of intermembrane space proteins such as cytochrome c
and Apaf1 into the cytosol where they activate the caspases and DNases that
execute cell death. The precise molecular components of the pore(s) responsible
for MOMP are unknown, but sphingolipids are thought to play a role. Here, we
review evidence for a role of sphingolipids in the induction of
mitochondrial-mediated apoptosis with a focus on potential underlying molecular
mechanisms by which altered sphingolipid metabolism indirectly or directly induce
MOMP. Data available on these mechanisms is reviewed, and the focus and
limitations of previous and current studies are discussed to present important
unanswered questions and potential future directions.
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