Journal of Immunology Research,
Journal Year:
2024,
Volume and Issue:
2024(1)
Published: Jan. 1, 2024
B
cells
are
essential
for
humoral
immune
response
due
to
their
ability
secrete
antibodies.
The
development
of
from
the
bone
marrow
periphery
is
tightly
regulated
by
a
complex
set
signals,
and
each
subset
has
unique
metabolic
profile.
Mitochondria,
which
serve
as
cellular
energy
powerhouses,
play
an
role
in
regulating
cell
survival
responses.
To
maintain
homeostasis,
mitochondria
dynamically
adjust
morphology,
distribution,
mass
via
biogenesis,
fusion
fission,
translocation,
mitophagy.
Despite
its
extreme
importance,
mitochondrial
quality
control
(MQC)
not
been
thoroughly
summarized,
unlike
T
cells.
This
article
aims
review
mechanism
MQC
that
shapes
fate
functions.
In
addition,
we
will
discuss
physiological
pathological
implications
cells,
providing
new
insights
into
potential
therapeutic
targets
diseases
associated
with
abnormalities.
Nature Communications,
Journal Year:
2025,
Volume and Issue:
16(1)
Published: Jan. 2, 2025
Abstract
Despite
the
enormous
significance
of
malaria
parasites
for
global
health,
some
basic
features
their
ultrastructure
remain
obscure.
Here,
we
apply
high-resolution
volumetric
electron
microscopy
to
examine
and
compare
transmissible
male
female
sexual
blood
stages
Plasmodium
falciparum
as
well
more
intensively
studied
asexual
revisiting
previously
described
phenomena
in
3D.
In
doing
so,
challenge
widely
accepted
notion
a
single
mitochondrion
by
demonstrating
presence
multiple
mitochondria
gametocytes.
We
also
provide
evidence
gametocyte-specific
cytostome,
or
cell
mouth.
Furthermore,
generate
first
3D
reconstructions
parasite’s
endoplasmic
reticulum
(ER)
Golgi
apparatus
gametocyte-induced
extraparasitic
structures
infected
red
cell.
Assessing
interconnectivity
between
organelles,
find
frequent
structural
appositions
nucleus,
mitochondria,
apicoplast.
that
ER
is
promiscuous
interactor
with
numerous
organelles
trilaminar
pellicle
gametocyte.
Public
availability
these
resources
will
facilitate
reinterrogation
others
different
research
questions
expertise.
Taken
together,
reconstruct
P.
gametocytes
at
nanometre
scale
shed
light
on
unique
organellar
biology
deadly
parasites.
International Journal of Molecular Sciences,
Journal Year:
2025,
Volume and Issue:
26(6), P. 2768 - 2768
Published: March 19, 2025
The
heart
requires
a
continuous
energy
supply
to
sustain
its
unceasing
contraction–relaxation
cycle.
Mitochondria,
double-membrane
organelle,
generate
approximately
90%
of
cellular
as
adenosine
triphosphate
(ATP)
through
oxidative
phosphorylation,
utilizing
the
electrochemical
gradient
established
by
respiratory
chain.
Mitochondrial
function
is
compromised
damage
mitochondrial
DNA,
including
point
mutations,
deletions,
duplications,
or
inversions.
Additionally,
disruptions
proteins
associated
with
membranes
regulating
metabolic
homeostasis
can
impair
chain’s
efficiency.
This
results
in
diminished
ATP
production
and
increased
generation
reactive
oxygen
species.
review
provides
an
overview
mutations
affecting
transporters
involved
synthesis,
particularly
those
synthesis
mobilization,
it
examines
their
role
pathogenesis
specific
cardiomyopathies.
Pharmacological Research,
Journal Year:
2024,
Volume and Issue:
205, P. 107235 - 107235
Published: May 28, 2024
Diabetic
cardiomyopathy
(DCM)
is
a
major
complication
of
diabetes
and
characterized
by
left
ventricular
dysfunction.
Currently,
there
lack
effective
treatments
for
DCM.
Ubiquitin-specific
protease
7
(USP7)
plays
key
role
in
various
diseases.
However,
whether
USP7
involved
DCM
has
not
been
established.
In
this
study,
we
demonstrated
that
was
upregulated
diabetic
mouse
hearts
NMCMs
co-treated
with
HG+PA
or
H9c2
cells
treated
PA.
Abnormalities
heart
morphology
function
were
reversed
silencing
through
conditional
gene
knockout
chemical
inhibition.
Proteomic
analysis
coupled
biochemical
validation
confirmed
PCG1β
one
the
direct
protein
substrates
aggravated
myocardial
damage
coactivation
PPARα
signaling
pathway.
restored
expression
fatty
acid
metabolism-related
proteins
mitochondrial
homeostasis
inhibiting
fission
promoting
fusion
events.
Similar
effects
also
observed
vitro.
Our
data
promoted
cardiometabolic
metabolism
disorders
dysfunction
via
stabilizing
suggested
may
be
therapeutic
strategy
iScience,
Journal Year:
2024,
Volume and Issue:
27(12), P. 111467 - 111467
Published: Nov. 23, 2024
The
MICOS
complex,
essential
for
cristae
organization,
comprises
MIC10
and
MIC60
subcomplexes,
with
MIC13
as
a
crucial
subunit.
mutations
cause
severe
mitochondrial
hepato-encephalopathy,
defects,
MIC10-subcomplex
loss.
We
demonstrate
that
depletion
of
the
protease
YME1L
in
KO
stabilizes
MIC10-subcomplex,
restoring
MIC60-MIC10
interaction
crista
junction
(CJ)
indicating
is
stabilization
rather
than
bridging.
identified
stomatin-like
protein
2
(SLP2)
key
partner,
morphology
CJ
formation.
SLP2
serves
an
hub
subunits
MIC26
by
protecting
it
from
YME1L-mediated
degradation.
Deleting
both
impairs
MIC60-subcomplex
assembly
its
nanoscale
organization.
Restoring
MIC13-SLP2
double
cells
through
reinstates
morphology.
Overall,
we
propose
act
proteolytically
controlled
'seeder'
facilitating
MICOS-MIB
complex
maintaining
integrity.
Cell Reports,
Journal Year:
2025,
Volume and Issue:
44(3), P. 115377 - 115377
Published: March 1, 2025
Cardiomyocytes
(CMs)
rely
on
mitochondrial
energy
produced
in
highly
interconnected
networks.
Direct
reprogramming
of
cardiac
fibroblasts
(CFs)
into
induced
CMs
(iCMs)
shows
promise
for
treating
injury,
but
little
work
has
investigated
energetics
and
morphology
during
the
conversion
CFs
to
iCMs.
We
characterized
mitochondria
direct
murine
neonatal
(mnCFs).
Reprogramming
increased
respiration
interconnectivity
not
levels
native
CMs.
therefore
whether
perturbations
dynamics
impacted
reprogramming.
Mitochondrial
fusion
(joining)
was
essential
iCM
generation,
while
various
fission
(dividing)
genes
were
barriers.
In
particular,
loss
regulator
1
like
(Mtfr1l)
significantly
yield
functionally
mature
iCMs
respiration.
These
changes
countered
by
concomitant
effector
optical
atrophy
protein
(Opa1).
The
present
study
advances
our
understanding
barriers
mechanisms
