The roles of mitochondria in global and local intracellular calcium signalling
Nature Reviews Molecular Cell Biology,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 27, 2025
Language: Английский
Ferroptosis: a novel mechanism of cell death in ophthalmic conditions
Yaqi Yang,
No information about this author
Yumeng Lin,
No information about this author
Zhongyu Han
No information about this author
et al.
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: June 27, 2024
Ferroptosis,
a
new
type
of
programmed
cell
death
proposed
in
recent
years,
is
characterized
mainly
by
reactive
oxygen
species
and
iron-mediated
lipid
peroxidation
differs
from
death,
such
as
apoptosis,
necrosis,
autophagy.
Ferroptosis
associated
with
variety
physiological
pathophysiological
processes.
Recent
studies
have
shown
that
ferroptosis
can
aggravate
or
reduce
the
occurrence
development
diseases
targeting
metabolic
pathways
signaling
tumors,
ischemic
organ
damage,
other
degenerative
related
to
peroxidation.
Increasing
evidence
suggests
closely
linked
onset
progression
various
ophthalmic
conditions,
including
corneal
injury,
glaucoma,
age-related
macular
degeneration,
diabetic
retinopathy,
retinal
detachment,
retinoblastoma.
Our
review
current
research
on
reveals
significant
advancements
our
understanding
pathogenesis,
aetiology,
treatment
these
conditions.
Language: Английский
Improving mitochondria-associated endoplasmic reticulum membranes integrity as converging therapeutic strategy for rare neurodegenerative diseases and cancer
Biochimica et Biophysica Acta (BBA) - Molecular Cell Research,
Journal Year:
2025,
Volume and Issue:
unknown, P. 119954 - 119954
Published: April 1, 2025
Language: Английский
Pathogenetic Involvement of Autophagy and Mitophagy in Primary Progressive Multiple Sclerosis
Journal of Cellular and Molecular Medicine,
Journal Year:
2025,
Volume and Issue:
29(8)
Published: April 1, 2025
ABSTRACT
Primary
progressive
multiple
sclerosis
(PPMS)
affects
a
subset
of
MS
patients
and
is
characterised
by
continuous
progression
from
the
onset.
The
molecular
mechanisms
underlying
PPMS
are
poorly
understood,
therapeutic
options
limited,
with
no
specific
markers
for
early
detection
monitoring.
This
study
investigated
roles
autophagy
mitophagy
in
PPMS.
We
found
that
(ATG5
ATG7)
(Parkin
Optineurin)
were
significantly
reduced
serum
compared
to
control
relapsing‐remitting
(RRMS)
individuals.
reduction
was
associated
an
increase
indicative
neurodegeneration
mitochondrial
dysfunction.
Additionally,
positive
correlation
between
proteins
group
suggests
these
reciprocally
modulated
Our
investigation
reveals
actively
involved
exhibit
distinct
patterns
across
subtypes.
Measurements
circulating
components
related
could
serve
as
potential
biomarkers
detection.
Language: Английский
Mitochondria–membranous organelle contacts at a glance
Journal of Cell Science,
Journal Year:
2025,
Volume and Issue:
138(9)
Published: May 1, 2025
ABSTRACT
Mitochondrial
contact
sites
are
specialized
interfaces
where
mitochondria
physically
interact
with
other
organelles.
Stabilized
by
molecular
tethers
and
defined
unique
proteomic
lipidomic
profiles,
these
enable
direct
interorganellar
communication
functional
coordination,
playing
crucial
roles
in
cellular
physiology
homeostasis.
Recent
advances
have
expanded
our
knowledge
of
site-resident
proteins,
illuminated
the
dynamic
adaptive
nature
interfaces,
clarified
their
contribution
to
pathophysiology.
In
this
Cell
Science
at
a
Glance
article
accompanying
poster,
we
summarize
mitochondrial
contacts
that
been
characterized
mammals,
mechanisms
underlying
formation,
principal
functions.
Language: Английский
Lhx6 deficiency causes human embryonic palatal mesenchymal cell mitophagy dysfunction in cleft palate
Haotian Luo,
No information about this author
Hio Cheng Ieong,
No information about this author
Runze Li
No information about this author
et al.
Molecular Medicine,
Journal Year:
2024,
Volume and Issue:
30(1)
Published: Oct. 22, 2024
Abstract
Background
Overconsumption
of
retinoic
acid
(RA)
or
its
analogues/derivatives
has
been
linked
to
severe
craniomaxillofacial
malformations,
such
as
cleft
palate
and
midface
hypoplasia.
It
noted
that
RA
disturbed
the
proliferation
migration
embryonic
palatal
mesenchymal
(EPM)
cells
in
these
yet
exact
mechanisms
underlying
disruptions
remained
unclear.
Methods
A
model
(RA)-induced
fetal
mice
was
successfully
established.
Histological
alterations
were
evaluated
using
Hematoxylin
Eosin
(H&E)
staining
RNA
situ
hybridization
(RNAscope).
Cellular
levels
quantified
via
Cell
Counting
Kit-8
(CCK-8)
assay
EdU
incorporation
assay,
while
cell
capabilities
investigated
wound
healing
Transwell
assays.
Mitochondrial
functions
assessed
through
Mito-Tracker
fluorescence,
mitochondrial
reactive
oxygen
species
(ROS)
measurement,
ATP
level
quantification,
DNA
(mtDNA)
copy
number
analysis.
Differential
gene
expression
associated
signaling
pathways
identified
bioinformatics
Alterations
transcriptional
translational
Lhx6
genes
with
mitophagy
quantitative
PCR
(qPCR)
Western
blot
analysis,
respectively.
morphology
autophagosomes
within
examined
transmission
electron
microscopy
(TEM).
Results
Abnormal
development
mice,
along
impaired
human
(HEPM)
cells,
affecting
function
concomitant
downregulation
Lhx6.
Knockdown
HEPM
resulted
altered
proliferation,
migration,
function.
Conversely,
aberrant
function,
observed
RA-induced
ameliorated
by
overexpression
Subsequent
research
demonstrated
dysfunction
modulating
PINK1/Parkin-mediated
mitophagy,
thereby
activating
MAPK
pathways.
Conclusion
is
essential
for
homeostasis
tuning
Downregulation
transcriptionally
disturbs
homeostasis,
which
turn
leads
defect
ultimately
causing
palate.
Graphical
abstract
Language: Английский
A deep phenotyping study in mouse and iPSC models to understand the role of oligodendroglia in optic neuropathy in Wolfram syndrome
Karan Ahuja,
No information about this author
Marjan Vandenabeele,
No information about this author
Fatemeharefeh Nami
No information about this author
et al.
Acta Neuropathologica Communications,
Journal Year:
2024,
Volume and Issue:
12(1)
Published: Aug. 28, 2024
Wolfram
syndrome
(WS)
is
a
rare
childhood
disease
characterized
by
diabetes
mellitus,
insipidus,
blindness,
deafness,
neurodegeneration
and
eventually
early
death,
due
to
autosomal
recessive
mutations
in
the
WFS1
(and
WFS2)
gene.
While
it
categorized
as
neurodegenerative
disease,
increasingly
becoming
clear
that
other
cell
types
besides
neurons
may
be
affected
contribute
pathogenesis.
MRI
studies
patients
phenotyping
WS
rodent
models
indicate
white
matter/myelin
loss,
implicating
role
for
oligodendroglia
WS-associated
neurodegeneration.
In
this
study,
we
sought
determine
if
are
whether
their
dysfunction
primary
cause
of
observed
optic
neuropathy
brain
We
demonstrate
7.5-month-old
Wfs1
Language: Английский
Unveiling ferroptosis: a new frontier in skin disease research
Ke Wang,
No information about this author
Yumeng Lin,
No information about this author
Dan Zhou
No information about this author
et al.
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: Oct. 4, 2024
Ferroptosis,
a
form
of
regulated
cell
death
distinct
from
apoptosis,
necrosis,
and
autophagy,
is
increasingly
recognized
for
its
role
in
skin
disease
pathology.
Characterized
by
iron
accumulation
lipid
peroxidation,
ferroptosis
has
been
implicated
the
progression
various
conditions,
including
psoriasis,
photosensitive
dermatitis,
melanoma.
This
review
provides
an
in-depth
analysis
molecular
mechanisms
underlying
compares
cellular
effects
with
other
forms
context
health
disease.
We
systematically
examine
five
specific
diseases,
ichthyosis,
polymorphous
light
eruption
(PMLE),
vitiligo,
melanoma,
detailing
influence
on
pathogenesis
progression.
Moreover,
we
explore
current
clinical
landscape
ferroptosis-targeted
therapies,
discussing
their
potential
managing
treating
diseases.
Our
aim
to
shed
therapeutic
modulating
research
practice.
Language: Английский