Brain Research Bulletin,
Journal Year:
2025,
Volume and Issue:
unknown, P. 111338 - 111338
Published: April 1, 2025
Acute
ischemic
stroke
(AIS)
is
a
focal
neurological
deficit
due
to
sudden
occlusion
of
cerebral
vessels
in
the
brain.
AIS-induced
neuronal
injury
and
associated
excite-toxicity
neurodegeneration
affect
synthesis
release
different
neurotrophic
factors
such
as
brain-derived
neurotropic
factor
(BDNF)
its
precursor
proBDNF.
Both
BDNF
proBDNF
act
on
specific
receptors
with
effects.
activates
tropomyosin
receptor
kinase
B
(TrkB)
results
promoting
survival,
synaptic
plasticity,
growth.
However,
p75
neurotrophin
(p75NTR)
sortilin
which
attenuates
plasticity
promotes
apoptosis.
Dysregulation
central
peripheral
expression
proBDNF/BDNF
linked
severity
clinical
outcomes
AIS.
Therefore,
this
review
aims
discuss
alterations
signaling
Findings
from
present
illustrated
that
proBDNF/p75NTR/sortilin
pathway
exaggerated
whereas;
BDNF-TrkB
reduced
AIS
leading
activation
signaling,
inhibition
could
be
promising
therapeutic
strategy
management
Immunity Inflammation and Disease,
Journal Year:
2023,
Volume and Issue:
11(4)
Published: April 1, 2023
Coronavirus
disease
2019
(Covid-19)
is
caused
by
a
novel
severe
acute
respiratory
syndrome
coronavirus
virus
type
2
(SARS-CoV-2)
leading
to
the
global
pandemic
worldwide.
Systemic
complications
in
Covid-19
are
mainly
related
direct
SARS-CoV-2
cytopathic
effects,
associated
hyperinflammation,
hypercytokinemia,
and
development
of
cytokine
storm
(CS).
As
well,
developed
due
propagation
oxidative
thrombotic
events
which
may
progress
state
called
(TS),
respectively.
In
addition,
inflammatory
lipid
storms
also
activation
cells
release
bioactive
lipids
correspondingly.
Therefore,
present
narrative
review
aimed
elucidate
interrelated
relationship
between
different
types
mixed
(MS).
conclusion,
infection
induces
various
including
CS,
storm,
TS
storm.
These
not
developing
alone
since
there
close
them.
MS
seems
be
more
appropriate
than
it
develops
intricate
interface
reactive
oxygen
species,
proinflammatory
cytokines,
complement
activation,
coagulation
disorders,
activated
signaling
pathway.
Cell Stress and Chaperones,
Journal Year:
2023,
Volume and Issue:
28(6), P. 657 - 673
Published: Oct. 5, 2023
Coronavirus
disease
2019
(COVID-19)
is
a
recent
pandemic
caused
by
novel
severe
acute
respiratory
syndrome
coronavirus
2
(SARS‑CoV‑2)
leading
to
pulmonary
and
extra-pulmonary
manifestations
due
the
development
of
oxidative
stress
(OS)
hyperinflammation.
The
underlying
cause
for
OS
hyperinflammation
in
COVID-19
may
be
related
inhibition
nuclear
factor
erythroid
2-related
(Nrf2),
master
regulator
antioxidative
responses
cellular
homeostasis.
Nrf2
pathway
inhibits
expression
pro-inflammatory
cytokines
cytokine
storm
COVID-19.
activators
can
attenuate
endothelial
dysfunction
(ED),
renin-angiotensin
system
(RAS)
dysregulation,
immune
thrombosis,
coagulopathy.
Hence,
this
review
aimed
reveal
potential
role
its
management
As
well,
we
tried
revise
mechanistic
Immunity Inflammation and Disease,
Journal Year:
2024,
Volume and Issue:
12(8)
Published: Aug. 1, 2024
Abstract
Background
Atherosclerosis
(AS)
is
a
progressive
disease
that
interferes
with
blood
flow,
leading
to
cardiovascular
complications
such
as
hypertension,
ischemic
heart
disease,
stroke,
and
vascular
ischemia.
The
progression
of
AS
correlated
inflammation,
oxidative
stress,
endothelial
dysfunction.
Various
signaling
pathways,
like
nuclear
erythroid‐related
factor
2
(Nrf2)
Kruppel‐like
(KLF2),
are
involved
in
the
pathogenesis
AS.
Nrf2
KLF2
have
anti‐inflammatory
antioxidant
properties.
Thus,
activation
these
pathways
may
reduce
development
Metformin,
an
insulin‐sensitizing
drug
used
management
type
diabetes
mellitus
(T2DM),
increases
expression
KLF2.
common
long‐term
macrovascular
complication
T2DM.
metformin,
through
its
pleiotropic
effect,
attenuate
Aims
Therefore,
this
review
aims
investigate
possible
role
metformin
concerning
effect
on
inhibition
reactive
oxygen
species
(ROS)
formation.
In
addition
antidiabetic
can
morbidities
mortalities
compared
other
agents,
even
similar
glucose
control
by
Nrf2/KLF2
pathway
activation.
Conclusion
conclusion,
effective
therapeutic
strategy
against
AS,
mainly
KLF2/Nrf2
axis.
European Journal of Neuroscience,
Journal Year:
2025,
Volume and Issue:
61(7)
Published: April 1, 2025
Multiple
sclerosis
(MS)
is
a
progressive
demyelinating
disease
of
the
CNS,
characterized
by
inflammation,
formation
CNS
plaques,
and
damage
to
neuronal
myelin
sheath
(Graphical
abstract).
Fibroblast
growth
factor
21
(FGF21)
involved
in
various
metabolic
disorders
neurodegenerative
diseases.
FGF21
its
co-receptor
β-Kloth
are
essential
remyelination
process
MS.
Metformin,
an
insulin-sensitizing
drug
that
first-line
treatment
for
type
2
diabetes
mellitus
(T2DM),
may
have
potential
neuroprotective
impact
up-regulating
production
FGF21,
which
prevent
onset
diseases
including
The
purpose
this
review
clarify
how
metformin
affects
MS
neuropathology
mechanistically
via
modifying
FGF21.
Metformin
increases
expression
also
β-Klotho,
modulates
oxidative
stress,
reduces
glutamate-induced
excitotoxicity,
regulates
platelet
function
coagulation
cascades.
In
conclusion,
can
enhance
functional
activity
counteracting
development
progression
Preclinical
clinical
studies
warranted
regard.
Brain Research Bulletin,
Journal Year:
2025,
Volume and Issue:
unknown, P. 111338 - 111338
Published: April 1, 2025
Acute
ischemic
stroke
(AIS)
is
a
focal
neurological
deficit
due
to
sudden
occlusion
of
cerebral
vessels
in
the
brain.
AIS-induced
neuronal
injury
and
associated
excite-toxicity
neurodegeneration
affect
synthesis
release
different
neurotrophic
factors
such
as
brain-derived
neurotropic
factor
(BDNF)
its
precursor
proBDNF.
Both
BDNF
proBDNF
act
on
specific
receptors
with
effects.
activates
tropomyosin
receptor
kinase
B
(TrkB)
results
promoting
survival,
synaptic
plasticity,
growth.
However,
p75
neurotrophin
(p75NTR)
sortilin
which
attenuates
plasticity
promotes
apoptosis.
Dysregulation
central
peripheral
expression
proBDNF/BDNF
linked
severity
clinical
outcomes
AIS.
Therefore,
this
review
aims
discuss
alterations
signaling
Findings
from
present
illustrated
that
proBDNF/p75NTR/sortilin
pathway
exaggerated
whereas;
BDNF-TrkB
reduced
AIS
leading
activation
signaling,
inhibition
could
be
promising
therapeutic
strategy
management
