Ask your competent? doctor to translate this word salad to layperson terms. Will something from here get survivors to 100% recovery?
Can kinase trafficking to mitochondria unlock new targets in ischemic stroke?
Stroke
is a major cause of death and permanent disability, which is described
by abrupt loss of neuronal energy, oxidative injury, inflammation, and
apoptosis, primarily mediated by mitochondrial dysfunction. Mitochondria
are key regulators of stress responses, apoptosis, redox homeostasis,
immune signaling and known as central signaling hubs, integrating
pathways from multiple cellular compartments to maintain homeostasis.
Among the major regulatory elements are protein kinase enzymes that
modulate cell signaling by phosphorylating substrates. Several kinases,
including members of the Akt, PKA, PKC, GSK-3β, PINK1, and MAPK
families, dynamically translocate to mitochondria under physiological
and pathological conditions. Once localized, they influence
mitochondrial dynamics, bioenergetics, reactive oxygen species (ROS)
production, and programmed cell death. Dysregulation of these functions
has been implicated in impaired mitophagy, aberrant calcium signaling,
and processes associated with the pathogenesis of various neurological
disorders, particularly in those with acute brain injuries,
such as acute ischemic stroke (AIS). Especially, mitochondrial kinase
oxidative stress hallmarks of neuronal injury. In this review, we
examine the role of mitochondrial-associated kinases in AIS, explore
mechanisms of their translocation, downstream signaling effects, and
their promise as druggable targets highlighting the importance of
spatial dynamics of kinases and the need for precision therapies.
Understanding these mechanisms may open new avenues for therapeutic
intervention in neurological diseases with a focus on acute brain
injury, by targeting mitochondrial signaling networks.
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