Restoring Mitochondrial Function and Muscle Satellite Cell Signaling: Remedies against Age-Related Sarcopenia
Biomolecules,
Journal Year:
2024,
Volume and Issue:
14(4), P. 415 - 415
Published: March 28, 2024
Sarcopenia
has
a
complex
pathophysiology
that
encompasses
metabolic
dysregulation
and
muscle
ultrastructural
changes.
Among
the
drivers
of
intracellular
changes
fibers
in
sarcopenia,
mitochondria
their
quality
control
pathways
play
relevant
roles.
Mononucleated
stem
cells/satellite
cells
(MSCs)
have
been
attributed
critical
role
repair
after
an
injury.
The
involvement
supporting
MSC-directed
is
unclear.
There
evidence
reduction
mitochondrial
biogenesis
blunts
repair,
thus
indicating
delivery
functional
to
injured
muscles
can
be
harnessed
limit
fibrosis
enhance
restoration
function.
Injection
autologous
respiration-competent
from
uninjured
sites
damaged
tissue
shown
reduce
infarct
size
cell
survival
preclinical
models
ischemia-reperfusion.
Furthermore,
incorporation
donor
into
MSCs
enhances
lung
cardiac
repair.
This
strategy
also
tested
for
regeneration
purposes
traumatic
injuries.
Indeed,
systemic
promotes
restores
mass
function
while
reducing
during
recovery
In
this
review,
we
discuss
contribution
altered
MSC
sarcopenia
illustrate
prospect
harnessing
as
therapeutic
against
age-related
sarcopenia.
Language: Английский
Mitochondrial dysfunction in pancreatic acinar cells: mechanisms and therapeutic strategies in acute pancreatitis
Fan Chen,
No information about this author
Kedong Xu,
No information about this author
Yimin Han
No information about this author
et al.
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: Dec. 24, 2024
Acute
pancreatitis
(AP)
is
an
inflammatory
disease
of
the
pancreas
and
a
complex
process
involving
multiple
factors,
with
mitochondrial
damage
playing
crucial
role.
Mitochondrial
dysfunction
now
considered
key
driver
in
development
AP.
This
often
presents
as
increased
oxidative
stress,
altered
membrane
potential
permeability,
DNA
mutations.
Under
stress
conditions,
dynamics
ROS
production
increase,
leading
to
decreased
potential,
imbalanced
calcium
homeostasis,
activation
permeability
transition
pore.
The
release
(mtDNA),
recognized
damage-associated
molecular
patterns,
can
activate
cGAS-STING1
NF-κB
pathway
induce
pro-inflammatory
factor
expression.
Additionally,
mtDNA
inflammasomes,
interleukin
subsequent
tissue
inflammation.
review
summarizes
relationship
between
mitochondria
AP
explores
protective
strategies
diagnosis
treatment
this
disease.
Future
research
on
acute
benefit
from
exploring
promising
avenues
such
antioxidants,
inhibitors,
new
therapies
that
target
dysfunction.
Language: Английский
Mechanism and prospects of mitochondrial transplantation for spinal cord injury treatment
Qin Wang,
No information about this author
Xin Wang,
No information about this author
Zhizhong Shang
No information about this author
et al.
Stem Cell Research & Therapy,
Journal Year:
2024,
Volume and Issue:
15(1)
Published: Nov. 28, 2024
Spinal
cord
injury
(SCI)
involves
a
continuous
and
dynamic
cascade
of
complex
reactions,
with
mitochondrial
damage
dysfunction-induced
energy
metabolism
disorders
playing
central
role
throughout
the
process.
These
not
only
determine
severity
secondary
injuries
but
also
influence
potential
for
axonal
regeneration.
Given
critical
disturbances
in
pathology
SCI,
strategies
such
as
enhancing
transport
within
axons
to
alleviate
local
deficits,
or
transplanting
autologous
allogeneic
mitochondria
restore
supply
damaged
tissues,
have
emerged
approaches
SCI
repair.
aim
modulate
inflammatory
responses
apoptosis.
Preclinical
studies
initially
demonstrated
that
transplantation
(MT)
significantly
reduces
neuronal
death
promotes
regeneration
following
spinal
injury.
MT
achieves
this
by
regulating
signaling
pathways
MAPK/ERK
PI3K/Akt,
promoting
expression
growth-associated
protein-43
(GAP-43)
neurons,
inhibiting
apoptosis-related
proteins
like
Grp78,
Chop,
P-Akt,
thereby
survival
neurons.
Additionally,
plays
vascular
endothelial
growth
factor,
facilitating
tissue
repair,
reducing
secretion
pro-inflammatory
cytokines
TNF-α,
IL-1β,
IL-6.
Furthermore,
modulates
apoptosis
decreasing
p-JNK,
member
MAPK
family.
In
summary,
reviewing
detailed
mechanisms
underlying
pathological
processes
we
emphasize
changes
endogenous
post-SCI
exogenous
This
review
aims
provide
insights
basis
developing
more
effective
clinical
treatments
SCI.
Language: Английский
Mitochondrial transplantation reconstructs the oxidative microenvironment within fibroblasts to reverse photoaging
Zihan Lu,
No information about this author
Wenhui Zhang,
No information about this author
Simo Wu
No information about this author
et al.
Biochemical and Biophysical Research Communications,
Journal Year:
2024,
Volume and Issue:
745, P. 151214 - 151214
Published: Dec. 19, 2024
Language: Английский
Enhanced lipid metabolism reprogramming in CHF rats through IL-6-mediated cardiac glial cell modulation by digilanid C and electroacupuncture stimulation combination
Yun Liu,
No information about this author
Xiao Sun,
No information about this author
Mingqian Yuan
No information about this author
et al.
Frontiers in Cell and Developmental Biology,
Journal Year:
2024,
Volume and Issue:
12
Published: Sept. 3, 2024
Background
Cardiac
lipid
metabolism
reprogramming
is
recognized
as
a
critical
pathological
factor
in
the
progression
of
chronic
heart
failure
(CHF).
The
therapeutic
potential
digilanid
C
and
electroacupuncture
stimulation
(ES)
enhancing
cardiac
function
has
been
established.
However,
optimal
synergistic
regulatory
strategies
these
interventions
on
have
yet
to
be
elucidated.
Methods
This
study
aimed
comprehensively
evaluate
impact
C-ES
combination
steatosis
remodeling
CHF.
Assessments
were
conducted
across
various
dimensions,
including
myocardial
oxygen
consumption,
mitochondrial
function,
metabolism.
Additionally,
we
sought
uncover
underlying
neuromolecular
mechanisms.
Results
Our
findings,
at
both
molecular
morphological
levels,
indicated
that
application
ES
significantly
inhibited
fibrosis
steatosis.
therapy
facilitated
repair
neuro-vascular
uncoupling
induced
Notably,
ameliorated
cardiomyocyte
apoptosis
enhanced
biogenesis
CHF,
leading
restructured
energy
supply
pattern.
immunofluorescence
analyses
revealed
aggregation
glial
cells
(CGCs)
sites
abnormal
neurovascular
coupling,
response
degeneration.
was
accompanied
by
marked
reduction
abnormally
elevated
expression
interleukin
6
(IL-6)
glutamatergic
signaling,
which
correlated
with
severity
aberrant
activation
CGCs.
combined
found
activate
Janus
kinase
1
(JAK1)/signal
transducer
activator
transcription
3
(STAT3)
pathway,
effectively
attenuated
accumulation
over-recruitment
CGCs
deprivation
nerves.
Conclusion
These
findings
underscore
novel
approach
modulate
complex
interplay
between
dynamics
metabolic
dysregulation
Language: Английский