Medicina,
Journal Year:
2025,
Volume and Issue:
61(2), P. 254 - 254
Published: Feb. 1, 2025
Nicotinamide
(NAM),
the
amide
form
of
vitamin
B3,
is
a
precursor
to
essential
cofactors
nicotinamide
adenine
dinucleotide
(NAD⁺)
and
NADPH.
NAD⁺
integral
numerous
cellular
processes,
including
metabolism
regulation,
ATP
production,
mitochondrial
respiration,
reactive
oxygen
species
(ROS)
management,
DNA
repair,
senescence,
aging.
NAM
supplementation
has
demonstrated
efficacy
in
restoring
energy,
repairing
damage,
inhibiting
inflammation
by
suppressing
pro-inflammatory
cytokines
release.
Due
its
natural
presence
variety
foods
excellent
safety
profile—even
at
high
doses
up
3
g/day—NAM
extensively
used
chemoprevention
non-melanoma
skin
cancers
treatment
dermatological
conditions
such
as
blistering
diseases,
atopic
dermatitis,
rosacea,
acne
vulgaris.
Recently,
anti-aging
properties
have
elevated
NAM’s
prominence
skincare
formulations.
Beyond
repair
energy
replenishment,
significantly
impacts
oxidative
stress
reduction,
cell
cycle
apoptosis
modulation.
Despite
these
multifaceted
benefits,
comprehensive
molecular
mechanisms
underlying
actions
remain
not
fully
elucidated.
This
review
consolidates
recent
research
shed
light
on
mechanisms,
emphasizing
critical
role
health
therapeutic
potential.
By
enhancing
our
understanding,
this
work
underscores
importance
continued
exploration
into
applications,
aiming
inform
future
clinical
practices
innovations.
ABSTRACT
Epidermal
melanocytes
form
synaptic‐like
contacts
with
cutaneous
nerve
fibers,
but
the
functional
outcome
of
these
connections
remains
elusive.
In
this
pilot
study
we
used
our
fully
humanized
re‐innervated
skin
organ
culture
model
to
investigate
melanocyte‐nerve
fiber
interactions
in
UV‐B‐induced
melanogenesis.
UV‐B‐irradiation
significantly
enhanced
melanin
content
and
tyrosinase
activity
compared
non‐innervated
controls,
indicating
that
neuronal
presence
is
essential
for
exacerbating
pigmentation
upon
UV‐B
irradiation
long‐term
culture.
Comparative
transcriptomic
analysis
between
laser‐capture‐microdissected
from
freshly
embedded
human
published
microarray
data
on
vitro
primary
identified
Semaphorin‐4A
(SEMA4A)
as
possible
mediator
fibers
interactions.
SEMA4A
protein
levels
Gp100
+
‐epidermal
were
higher
skin,
reduced
by
treatment.
Analysis
showed
expression
24
h
after
while
secretion
into
medium
was
increased.
Beta‐tubulin
axon
growth
sensory
neurons
stimulated
conditioned
media
(CM)
irradiated
melanocytes.
When
neuronal‐conditioned
transferred
fresh
melanocytes,
increased,
only
if
had
been
treated
CM
These
findings
highlight
importance
melanocyte‐neuron
melanogenesis
suggest
secreted
proteins
(e.g.,
SEMA4A)
can
function
a
novel
target
treat
hypo‐
hyperpigmentation
disorders.
Experimental Dermatology,
Journal Year:
2025,
Volume and Issue:
34(2)
Published: Jan. 30, 2025
ABSTRACT
Glucocorticoids
(GCs)
are
synthesised
de
novo
by
peripheral
tissues
and
the
adrenal
cortex
of
hypothalamic–pituitary–adrenal
axis.
Skin
expresses
an
enzyme
called
11β‐hydroxysteroid
dehydrogenase
type
1
(11β‐HSD1),
which
reduces
cortisone
to
active
hormone
cortisol
activates
GC
receptors.
11β‐HSD1
plays
a
significant
role
in
alleviating
atopic
inflammation
through
elevation
concentrations
skin.
This
study
aimed
investigate
diosmetin
as
activator
(11β‐HSD1).
In
human
keratinocytes,
was
found
upregulate
protein
expression
levels,
well
transcriptional
mRNA.
However,
this
upregulation
mRNA
abrogated
keratinocytes
transfected
with
small
interfering
RNA
(siRNA).
dermatitis
(AD)
murine
model,
topical
administration
significantly
attenuated
basal
transepidermal
water
loss
(TEWL)
Eczema
Area
Severity
Index
(EASI),
while
enhancing
stratum
corneum
(SC)
hydration.
Diosmetin
also
increased
corticosterone
levels
SC
upregulated
both
serum
epidermis.
Furthermore,
treatment
led
marked
reduction
immunoglobulin
E
(IgE)
tumour
necrosis
factor‐α
(TNF‐α)
suppressed
thymic
stromal
lymphopoietin
(TSLP),
interleukin‐1β
(IL‐1β),
IL‐4,
IL‐13
Collectively,
these
findings
suggest
that
promotes
endogenous
activation
glucocorticoids
via
local
activation,
underscoring
its
potential
novel
therapeutic
agent
for
management
inflammatory
skin
disorders,
such
AD.
Medicina,
Journal Year:
2025,
Volume and Issue:
61(2), P. 254 - 254
Published: Feb. 1, 2025
Nicotinamide
(NAM),
the
amide
form
of
vitamin
B3,
is
a
precursor
to
essential
cofactors
nicotinamide
adenine
dinucleotide
(NAD⁺)
and
NADPH.
NAD⁺
integral
numerous
cellular
processes,
including
metabolism
regulation,
ATP
production,
mitochondrial
respiration,
reactive
oxygen
species
(ROS)
management,
DNA
repair,
senescence,
aging.
NAM
supplementation
has
demonstrated
efficacy
in
restoring
energy,
repairing
damage,
inhibiting
inflammation
by
suppressing
pro-inflammatory
cytokines
release.
Due
its
natural
presence
variety
foods
excellent
safety
profile—even
at
high
doses
up
3
g/day—NAM
extensively
used
chemoprevention
non-melanoma
skin
cancers
treatment
dermatological
conditions
such
as
blistering
diseases,
atopic
dermatitis,
rosacea,
acne
vulgaris.
Recently,
anti-aging
properties
have
elevated
NAM’s
prominence
skincare
formulations.
Beyond
repair
energy
replenishment,
significantly
impacts
oxidative
stress
reduction,
cell
cycle
apoptosis
modulation.
Despite
these
multifaceted
benefits,
comprehensive
molecular
mechanisms
underlying
actions
remain
not
fully
elucidated.
This
review
consolidates
recent
research
shed
light
on
mechanisms,
emphasizing
critical
role
health
therapeutic
potential.
By
enhancing
our
understanding,
this
work
underscores
importance
continued
exploration
into
applications,
aiming
inform
future
clinical
practices
innovations.