Cells,
Journal Year:
2024,
Volume and Issue:
13(17), P. 1453 - 1453
Published: Aug. 29, 2024
This
review
delves
into
the
molecular
complexities
underpinning
epithelial-to-mesenchymal
transition
(EMT)
induced
by
cigarette
smoke
(CS)
in
human
bronchial
epithelial
cells
(HBECs).
The
complex
interplay
of
pathways,
including
those
related
to
WNT//β-catenin,
TGF-β/SMAD,
hypoxia,
oxidative
stress,
PI3K/Akt,
and
NF-κB,
plays
a
central
role
mediating
this
transition.
While
these
findings
significantly
broaden
our
understanding
CS-induced
EMT,
research
reviewed
herein
leans
heavily
on
2D
cell
cultures,
highlighting
gap.
Furthermore,
identifies
stark
omission
genetic
epigenetic
factors
recent
studies.
Despite
shortcomings,
furnish
consolidated
foundation
not
only
for
academic
community
but
also
broader
scientific
industrial
sectors,
large
tobacco
companies
manufacturers
products,
both
areas
current
identifying
deeper
exploration.
synthesis
aims
propel
further
research,
hoping
unravel
EMT
context
CS
exposure.
expands
reveals
critical
limitations
methodologies,
primarily
reliance
which
may
adequately
simulate
more
biological
interactions.
Additionally,
it
highlights
significant
gap
literature
concerning
involved
suggesting
an
urgent
need
comprehensive
studies
that
incorporate
types
experiments.
Bulletin of the National Research Centre/Bulletin of the National Research Center,
Journal Year:
2024,
Volume and Issue:
48(1)
Published: Jan. 22, 2024
Abstract
Background
Tobacco
smoking
remains
a
major
preventable
cause
of
disease
and
death
worldwide.
Combustible
cigarettes
release
thousands
chemicals
that
can
initiate
inflammatory
pathways
leading
to
smoking-related
illness.
This
review
aims
synthesize
current
scientific
knowledge
on
mechanisms
smoking-induced
disease,
epidemiological
trends,
clinical
strategies
from
recent
literature.
Main
body
the
abstract
At
cellular
level,
cigarette
smoke
triggers
oxidative
stress
through
reactive
oxygen
species
(ROS),
causing
DNA
damage.
provokes
signaling
cascades
mediated
by
damage-associated
molecular
patterns
(DAMPs),
receptors
like
RAGE
TLRs,
downstream
cytokines.
Smoking
also
disrupts
apoptosis
autophagy.
In
lungs,
inflammation
play
central
roles
in
COPD
pathogenesis.
Smoking-induced
damage,
chronic
inflammation,
impaired
immunity
combine
promote
lung
carcinogenesis.
For
cardiovascular
endothelial
dysfunction,
platelet
activation,
atherogenesis
oxidized
LDL
effects
nitric
oxide
adhesion
molecules.
Short
conclusion
Given
unequivocal
evidence
health
risks,
cessation
is
critical
reducing
disability.
Both
counseling
pharmacotherapy
have
proven
efficacy
for
quitting,
but
limited
long-term.
Emerging
nicotine
products
e-cigarettes
unknown
impacts
population
health.
Comprehensive
efforts
encompassing
prevention,
screening,
treatment
innovation,
harm
reduction,
policy
reform
focused
curbing
smoking-attributable
morbidity
mortality
are
warranted.
Antioxidants,
Journal Year:
2024,
Volume and Issue:
13(1), P. 98 - 98
Published: Jan. 14, 2024
Inflammation
is
a
vital
defense
mechanism,
creating
hostile
conditions
for
pathogens,
preventing
the
spread
of
tissue
infection
and
repairing
damaged
tissues
in
humans
animals.
However,
when
inflammation
resolution
delayed
or
compromised
as
result
its
misregulation,
process
proceeds
from
acute
phase
to
chronic
inflammation,
leading
development
various
illnesses.
It
proven
that
redox
balance
disturbances
oxidative
stress
are
among
major
factors
inducing
NF-κB
over-inflammation.
Therefore,
anti-inflammatory
properties
natural
antioxidants
have
been
widely
tested
vitro
vivo
systems.
Accumulating
evidence
indicates
silymarin
(SM)
main
constituent
silibinin/silybin
(SB)
great
potential
an
anti-inflammation
agent.
The
mechanism
SM/SB
action
attributed
inhibition
TLR4/NF-κB-mediated
signaling
pathways
downregulated
expression
pro-inflammatory
mediators,
including
TNF-α,
IL-1β,
IL-6,
IL-12,
IL-23,
CCL4,
CXCL10,
etc.
Of
note,
same
model
systems,
was
able
upregulate
cytokines
(IL-4,
IL-10,
IL-13,
TGF-β,
etc.)
lipid
mediators
involved
inflammation.
inflammatory
were
clearly
demonstrated
systems
based
on
immune
(macrophages
monocytes)
non-immune
(epithelial,
skin,
bone,
connective
cancer)
cells.
At
time,
confirmed
number
models,
toxicity
nonalcoholic
fatty
liver
disease,
ischemia/reperfusion
stress-induced
injuries,
ageing
exercising
wound
healing
many
other
relevant
seems
likely
activities
key
elements
health-promoting
these
phytochemicals.
Science Progress,
Journal Year:
2024,
Volume and Issue:
107(4)
Published: Oct. 1, 2024
The
incidence
of
cancer
is
increasing
and
evolving
as
a
major
source
mortality.
Nanotechnology
has
garnered
considerable
scientific
interest
in
recent
decades
can
offer
promising
solution
to
the
challenges
encountered
with
traditional
chemotherapy.
Nanoparticle
utilization
holds
promise
combating
other
diseases,
offering
exciting
prospects
for
drug
delivery
systems
medicinal
applications.
Metallic
nanoparticles
exhibit
remarkable
physical
chemical
properties,
such
their
minute
size,
composition,
structure,
extensive
surface
area,
rendering
them
versatile
cost-effective.
Research
demonstrated
significant
beneficial
impact
on
treatment,
characterized
by
enhanced
targeting
abilities,
gene
activity
suppression,
improved
efficiency.
By
incorporating
ligands,
functionalized
metal
ensure
precise
energy
deposition
within
tumors,
thereby
augmenting
treatment
accuracy.
Moreover,
beyond
therapeutic
efficacy,
serve
valuable
tools
cell
visualization,
contributing
diagnostic
techniques.
Utilizing
allows
simultaneous
diagnosis
while
also
facilitating
controlled
release,
thus
revolutionizing
care.
This
narrative
review
investigates
advancements
types
mechanisms
cells,
application
clinical
scenarios,
potential
toxicity
medicine.
Turkish Journal of Biochemistry,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 6, 2025
Abstract
Objectives
This
study
aims
to
investigate
the
effect
of
smoking
on
metabolism
kynurenine
and
thus
contribute
elucidation
potential
mechanism
cigarette
smoking.
Methods
The
included
82
smokers
63
nonsmokers
who
applied
Family
Medicine
Polyclinic
for
routine
check-ups.
Sociodemographic
data,
laboratory
results,
Framingham
risk
scores
(FRS),
Fagerström
Nicotine
Dependence
Test
(FTND)
were
recorded.
Serum
tryptophan,
kynurenine,
kynurenic
acid,
3-hydroxyanthranilic
3-hydroxykynurenine,
quinolinic
acid
concentrations
measured
with
tandem
mass
spectrometry.
Results
tryptophan
levels
(p=0.040)
statistically
significantly
lower
in
smokers,
kynurenine/tryptophan
ratio
serum
higher
(p<0.001).
correlation
analysis
smoker
group
showed
a
positive
between
FTDN.
positively
correlated
total
cholesterol,
triglyceride,
low-density
lipoprotein
FRS.
There
was
participants’
systolic
diastolic
blood
pressures.
Conclusions
Our
findings
that
via
pathway
induced
smokers.
International Journal of Molecular Sciences,
Journal Year:
2025,
Volume and Issue:
26(1), P. 333 - 333
Published: Jan. 2, 2025
The
red
blood
cell
(RBC)
membrane
is
unique
and
crucial
for
maintaining
structural–functional
relationships.
Maternal
smoking
induces
significant
changes
in
the
morphological,
rheological,
functional
parameters
of
both
maternal
foetal
RBCs,
mainly
due
to
continuous
generation
free
radicals.
major
aim
this
study
was
follow
consequences
a
secondary
stressor,
like
fungal
infection,
on
already
compromised
RBC
populations.
impact
Candida
growing
health
concern,
investigated
four
sample
groups:
mothers
their
neonates
originating
from
non-smoking
versus
Here,
we
searched
phenotypical
molecular
markers
that
precisely
reflected
effect
infection
membrane;
included
level
hemolysis,
appearance
morphological
variants,
formation
lipid
peroxidation
marker
4-hydroxyl-nonenal,
arrangement
Band
3
molecules
activation
Caspase
3.
In
most
examined
cases,
increased
adverse
symptoms
induced
by
smoking,
indicating
general
stress
response,
likely
an
altered
redox
state
cells.
However,
were
able
identify
atypical
phenotype
(clustered
populations
with
shrinkage
blebbing)
populations,
which
might
be
spp.
infection.
Biomolecules and Biomedicine,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 17, 2025
In
recent
years,
the
health
challenges
linked
to
frailty
in
elderly,
particularly
those
worsened
by
cigarette
smoke,
have
become
more
pronounced.
However,
quantitative
studies
examining
impact
of
smoking
dosage
on
this
population
remain
limited.
To
address
gap,
we
developed
a
model
using
smoke-exposed
elderly
mice.
Fifteen-month-old
C57BL/6J
mice
were
exposed
smoke
from
two
burning
cigarettes
for
15
min
whole-body
chamber.
This
exposure
occurred
4,
6,
and
8
times
daily
30
days,
representing
low,
medium,
high
dosages,
respectively.
Frailty
levels
assessed
through
rotation
grip
strength
tests,
alongside
lung
histopathology
inflammatory
factor
protein
expression
analyses
across
three
groups.
Additionally,
used
Gene
Expression
Omnibus
(GEO)
database
validate
correlation
between
inflammation
smokers,
facilitating
cross-comparisons
animal
findings
human
sample
data.
Our
results
show
that
high-dose
significantly
prone
frailty,
with
notable
reductions
maximal
(P
<
0.01)
drop
time
0.001).
Among
samples,
69.2%
smokers
exhibited
phenotype,
compared
just
15.4%
nonsmokers.
Both
smoking-exposed
demonstrated
upregulation
tumor
necrosis
factor-α
(TNF-α)
interleukin-1
β
(IL-1β)
tissue
serum.
Mechanistically,
activates
NF-κB
signaling
pathway.
quantitatively
link
smoking-induced
increased
TNF-α
IL-1β,
providing
experimental
evidence
diagnosis
prevention
populations.
Expert Review of Respiratory Medicine,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Feb. 13, 2025
Introduction
Idiopathic
pulmonary
fibrosis
(IPF)
isa
chronic,
progressive
lung
disease
characterized
by
distorted
alveolar
structureand
reduced
compliance,
and
impaired
ventilation-perfusion.
Small
airwaydisease
(SAD)
is
often
termed
a
'quietzone'
due
to
its
asymptomatic
nature.
Around
30-40%
of
IPF
patients
exhibit
SAD,which
associated
with
worse
prognosis,
higher
emphysema
scores,and
elevated
mortality
risk.
We
used
PubMed
Google
Scholar
for
literaturesearch.
Cardiovascular Diabetology,
Journal Year:
2025,
Volume and Issue:
24(1)
Published: March 24, 2025
The
American
Heart
Association
(AHA)
proposed
the
concept
of
cardiovascular–kidney–metabolic
(CKM)
syndrome,
underscoring
interconnectedness
cardiovascular,
renal,
and
metabolic
diseases.
stress
hyperglycemia
ratio
(SHR)
represents
an
innovative
indicator
that
quantifies
blood
glucose
fluctuations
in
patients
experiencing
acute
or
subacute
stress,
correlating
with
detrimental
clinical
effects.
Nevertheless,
prognostic
significance
SHR
within
individuals
diagnosed
CKM
syndrome
stages
0
to
3,
particularly
respect
all-cause
cardiovascular
disease
(CVD)
mortality
risks,
has
not
been
fully
understood
yet.
current
study
analyzed
data
from
9647
participants
covering
based
on
NHANES
(National
Health
Nutrition
Examination
Survey)
collected
2007
2018.
In
this
study,
primary
exposure
variable
was
SHR,
computed
as
fasting
plasma
divided
by
(1.59
*
HbA1c
−
2.59).
main
endpoints
were
well
CVD
mortality,
death
registration
sourced
through
December
31,
2019.
CHARLS
database
(China
Retirement
Longitudinal
Study)
utilized
validation
enhance
reliability
findings.
This
included
participants,
who
followed
for
a
median
duration
6.80
years.
During
period,
630
cases
135
CVD-related
deaths
total
recorded.
After
full
adjustment
covariates,
our
results
displayed
robust
positive
association
(Hazard
[HR]
=
1.09,
95%
Confidence
interval
[CI]
1.04–1.13).
However,
exhibited
no
significant
relationship
(HR
1.00,
CI
0.91–1.11).
mediation
analysis
suggested
between
risk
is
partially
mediated
RDW,
albumin,
RAR.
Specifically,
mediating
effects
17.0%
(95%
46.7%,
8.7%),
10.1%
23.9%,
4.7%),
23.3%
49.0%,
13.0%),
respectively.
Additionally,
analyses
indicated
correlation
among
across
0–3
during
follow-up
period
2011
2020.
An
increased
value
positively
associated
elevated
likelihood
0–3,
yet
it
shows
mortality.
important
tool
predicting
long-term
adverse
outcomes
population.
Cardiovascular–kidney–metabolic
emphasizes
kidney,
novel
marker
reflecting
stress-induced
fluctuations,
but
its
(stages
0–3)
remains
uncertain.
explores
Our
findings
indicate
significantly
1.04–1.13),
CI:
Mediation
Validation
using
supports
these
These
suggest
could
serve
biomarker
patients,
offering
potential
utility
stratification
management.