International Journal of Biological Sciences,
Journal Year:
2024,
Volume and Issue:
21(2), P. 475 - 489
Published: Dec. 31, 2024
As
a
leading
cause
of
morbidity
and
mortality,
fibrosis
is
the
common
pathway
various
chronic
inflammatory
diseases
in
organs
causes
death
large
number
patients.
It
can
destroy
structure
function
ultimately
lead
to
organ
failure,
which
major
disability
many
diseases.
However,
regulatory
mechanism
not
well
clear
lack
effective
drugs
treatments,
seriously
endangers
human
health
safety.
In
this
study,
we
found
that
ubiquitin
specific
peptidases
25
(USP25)
deficiency
could
protect
mice
from
bleomycin
(BLM)-induced
pulmonary
bile
duct
ligation
(BDL)-induced
liver
fibrosis.
Mechanistically,
USP25
reduced
infiltration
M2
macrophages
lungs
livers.
inhibits
signal
transducer
activator
transcription
6
/
peroxisome
proliferator-activated
receptor
gamma
(STAT6/PPAR-γ)
signaling
by
reducing
K48
ubiquitination
STAT6,
thereby
promoting
IL-4-induced
macrophages.
Overall,
our
findings
support
promotes
development
facilitating
macrophage
polarization.
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: July 26, 2024
Idiopathic
pulmonary
fibrosis
(IPF)
is
a
lung
disease
that
worsens
over
time,
causing
in
the
lungs
and
ultimately
resulting
respiratory
failure
high
risk
of
death.
Macrophages
play
crucial
role
immune
system,
showing
flexibility
by
transforming
into
either
pro-inflammatory
(M1)
or
anti-inflammatory
(M2)
macrophages
when
exposed
to
different
stimuli,
impacting
development
IPF.
Recent
research
has
indicated
polarization
onset
progression
M1
secrete
inflammatory
cytokines
agents
early
damage
fibrosis,
while
M2
support
tissue
healing
releasing
cytokines.
Developing
novel
treatments
for
IPF
relies
on
thorough
comprehension
processes
involved
macrophage
The
review
outlines
regulation
its
impact
IPF,
with
goal
investigating
possible
therapeutic
benefits
advancement
ACS Nano,
Journal Year:
2025,
Volume and Issue:
unknown
Published: April 4, 2025
Tendon
repair
remains
challenging
owing
to
the
limited
capacity
for
endogenous
repair.
Vasoactive
intestinal
peptide
(VIP)
promotes
bone
tissue
regeneration;
however,
its
role
in
tendon
unclear.
In
present
study,
we
demonstrated
that
VIP
stimulated
M2
polarization
of
macrophages
and
facilitated
regeneration
by
regulating
immune
homeostasis
maintaining
function
stem/progenitor
cells
(TSPCs).
Additionally,
established
GelMa-loaded
VIP@PLGA@ZIF-8
(VPZ)
nanoparticles
(VPZG)
enable
sustained
localized
release
at
site
patellar
injury
SD
rats.
The
results
vitro
experiments
VPZG
regulated
macrophage
downregulating
NF-κB
axis.
also
promoted
efferocytosis
suppressed
proinflammatory
factors.
enhanced
tenogenic
differentiation
TSPCs
when
cocultured
with
macrophages.
vivo,
implanted
injury,
where
it
released
sustainably
slowly
promote
regeneration.
This
effect
was
achieved
through
downregulation
expression
levels
various
inflammatory
factors,
as
well
regulation
local
homeostasis.
conclusion,
our
enhancing
TSPC
function.
These
findings
suggest
is
a
promising
avenue
clinical
improvement
treatment.
Advanced Science,
Journal Year:
2025,
Volume and Issue:
unknown
Published: May 19, 2025
Abstract
Fibrotic
skin
diseases
are
characterized
by
excessive
fibroblast
proliferation
and
pathological
extracellular
matrix
deposition.
As
a
pivotal
coenzyme
in
cellular
energetics,
NAD
homeostasis
perturbation
is
implicated
fibrosis.
Multiple
studies
have
demonstrated
the
therapeutic
potential
of
mesenchymal
stem
cells
(MSCs)
against
cutaneous
fibrosis,
while
specific
mechanism
remains
elusive.
Herein,
this
work
finds
that
although
almost
all
MSCs
undergo
situ
apoptosis
within
24
h
post‐subcutaneous
administration,
MSC‐derived
apoptotic
bodies
(ABs)
mediated
potent
anti‐fibrotic
effects.
Mechanistically,
ABs
can
restore
mitochondrial
through
NAMPT
transfer,
FOXO1
deacetylation
enhancement,
PINK1/PARKIN‐dependent
mitophagy
activation.
To
achieve
penetration
into
hard
fibrotic
skin,
permeable
(pABs)
constructed
via
metabolic
glycoengineering
copper‐free
click
chemistry
techniques.
In
both
keloid
xenograft
scleroderma
murine
models,
pABs
significantly
penetrate
collagen
reduce
summary,
research
establishes
highly
promising
strategy
for
reversing
fibrosis
with
matrix.
Frontiers in Medicine,
Journal Year:
2024,
Volume and Issue:
11
Published: Nov. 27, 2024
Background
Extensive
research
has
examined
the
role
of
metabolism
in
lung
disease
development,
yet
a
comprehensive
literature
review
remains
absent
despite
numerous
publications.
Objective
This
study
aims
to
visualize
and
assess
advancements
on
its
diseases.
Methods
Publications
from
January
1,
1991,
April
30,
2024,
related
diseases
were
sourced
Web
Science
Core
Collection
analyzed
using
CiteSpace
6.2.R4,
VOSviewer
1.6.19,
Bibliometrix,
R
Studio,
various
online
tools.
Results
A
total
1,542
studies
collected
processed
through
these
platforms
for
analysis
data
visualization.
The
revealed
sharp
increase
annual
publications
diseases,
with
United
States
China
emerging
as
leading
contributors.
Current
trends
highlight
shift
toward
investigating
metabolic
reprogramming
immune
cells
context
Moreover,
genes
such
TNF,
DIF,
AKT1,
INS,
IL-6,
CXCL8,
IL-1β,
TP53,
NF-κB1,
MTOR,
IFNG,
TGF-β1,
HIF1α,
VEGFA,
IL-10,
NFE2L2,
PPARG,
AKT,
CRP,
STAT3,
CD4
have
received
significant
attention
this
domain.
Employing
bibliometric
approach,
offers
objective
examination
knowledge
landscape,
shedding
light
evolving
field.
findings
serve
valuable
resource
researchers,
offering
clearer
perspective
metabolism-related
studies.
