Cell Death and Disease,
Journal Year:
2024,
Volume and Issue:
15(6)
Published: June 28, 2024
Abstract
S100a8/a9,
largely
released
by
polymorphonuclear
neutrophils
(PMNs),
belongs
to
the
S100
family
of
calcium-binding
proteins
and
plays
a
role
in
variety
inflammatory
diseases.
Although
S100a8/a9
has
been
reported
trigger
endothelial
cell
apoptosis,
mechanisms
S100a8/a9-induced
dysfunction
during
sepsis
require
in-depth
research.
We
demonstrate
that
high
expression
levels
suppress
Ndufa3
mitochondrial
complex
I
via
downregulation
Nrf1
expression.
Mitochondrial
deficiency
contributes
NAD
+
-dependent
Sirt1
suppression,
which
induces
disorders,
including
excessive
fission
blocked
mitophagy,
mtDNA
from
damaged
mitochondria
ultimately
activates
ZBP1-mediated
PANoptosis
cells.
Moreover,
based
on
comprehensive
scRNA-seq
bulk
RNA-seq
analyses,
S100A8/A9
hi
are
closely
associated
with
circulating
count
(a
useful
marker
damage),
S100A8
is
an
independent
risk
factor
for
poor
prognosis
patients.
Autophagy,
Journal Year:
2023,
Volume and Issue:
20(2), P. 221 - 241
Published: Sept. 12, 2023
Non-alcoholic
fatty
liver
disease
(NAFLD)
is
one
of
the
most
common
chronic
diseases
with
a
global
rising
prevalence,
which
closely
associated
high-fat
diet
(HFD)
intake.
Macroautophagy/autophagy
an
evolutionarily
conserved
degradation
process
for
cytosolic
macromolecules
and
damaged
organelles.
The
potential
role
autophagy
in
hepatic
lipid
metabolism
has
been
recognized,
while
dysfunction
found
to
contribute
NAFLD.
Herein,
we
provide
overview
phases
regulatory
machinery,
current
understanding
its
protective
HFD-induced
We
also
discuss
genetic
pharmacological
interventions
that
may
help
elucidate
molecular
mechanisms
influence
future
therapeutic
direction
Annual Review of Physiology,
Journal Year:
2024,
Volume and Issue:
86(1), P. 225 - 253
Published: Feb. 12, 2024
Exosomes
are
small
extracellular
vesicles
that
carry
lipids,
proteins,
and
microRNAs
(miRNAs).
They
released
by
all
cell
types
can
be
found
not
only
in
circulation
but
many
biological
fluids.
essential
for
interorgan
communication
because
they
transfer
their
contents
from
donor
to
recipient
cells,
modulating
cellular
functions.
The
miRNA
content
of
exosomes
is
responsible
most
effects,
changes
exosomal
levels
contribute
the
progression
or
regression
metabolic
diseases.
As
miRNAs
selectively
sorted
packaged
into
exosomes,
useful
as
biomarkers
diagnosing
field
metabolism
expanding
rapidly,
researchers
consistently
making
new
discoveries
this
area.
a
result,
have
great
potential
next-generation
drug
delivery
platform
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: May 21, 2024
The
skin,
being
a
multifaceted
organ,
performs
pivotal
function
in
the
complicated
wound-healing
procedure,
which
encompasses
triggering
of
several
cellular
entities
and
signaling
cascades.
Aberrations
typical
healing
process
wounds
may
result
atypical
scar
development
establishment
persistent
condition,
rendering
patients
more
vulnerable
to
infections.
Chronic
burns
have
detrimental
effect
on
overall
quality
life
patients,
resulting
higher
levels
physical
discomfort
socio-economic
complexities.
occurrence
frequency
prolonged
are
rise
as
aging
people,
hence
contributing
escalated
expenditures
within
healthcare
system.
clinical
evaluation
treatment
chronic
continue
pose
challenges
despite
advancement
different
therapeutic
approaches.
This
is
mainly
owing
duration
intricate
processes
involved
wound
healing.
Many
conventional
methods,
such
administration
growth
factors,
use
dressings,
application
skin
grafts,
used
ease
across
diverse
types.
Nevertheless,
these
approaches
only
be
practical
for
some
wounds,
highlighting
need
advance
alternative
modalities.
Novel
care
technologies,
nanotherapeutics,
stem
cell
treatment,
3D
bioprinting,
aim
improve
efficacy,
prioritize
regeneration,
minimize
adverse
effects.
review
provides
an
updated
overview
recent
advancements
management
using
innovative
Cell Death and Disease,
Journal Year:
2024,
Volume and Issue:
15(6)
Published: June 28, 2024
Abstract
S100a8/a9,
largely
released
by
polymorphonuclear
neutrophils
(PMNs),
belongs
to
the
S100
family
of
calcium-binding
proteins
and
plays
a
role
in
variety
inflammatory
diseases.
Although
S100a8/a9
has
been
reported
trigger
endothelial
cell
apoptosis,
mechanisms
S100a8/a9-induced
dysfunction
during
sepsis
require
in-depth
research.
We
demonstrate
that
high
expression
levels
suppress
Ndufa3
mitochondrial
complex
I
via
downregulation
Nrf1
expression.
Mitochondrial
deficiency
contributes
NAD
+
-dependent
Sirt1
suppression,
which
induces
disorders,
including
excessive
fission
blocked
mitophagy,
mtDNA
from
damaged
mitochondria
ultimately
activates
ZBP1-mediated
PANoptosis
cells.
Moreover,
based
on
comprehensive
scRNA-seq
bulk
RNA-seq
analyses,
S100A8/A9
hi
are
closely
associated
with
circulating
count
(a
useful
marker
damage),
S100A8
is
an
independent
risk
factor
for
poor
prognosis
patients.
