International Journal of Molecular Sciences,
Journal Year:
2021,
Volume and Issue:
22(5), P. 2715 - 2715
Published: March 8, 2021
Cardiovascular
disease
is
the
leading
cause
of
mortality
and
morbidity
around
globe,
creating
a
substantial
socio-economic
burden
as
result.
Myocardial
infarction
significant
contributor
to
detrimental
impact
cardiovascular
disease.
The
death
cardiomyocytes
following
myocardial
causes
an
immune
response
which
leads
further
destruction
tissue,
subsequently,
results
in
formation
non-contractile
scar
tissue.
Macrophages
have
been
recognized
important
regulators
participants
inflammation
fibrosis
infarction.
are
generally
classified
into
two
distinct
groups,
namely,
classically
activated,
or
M1
macrophages,
alternatively
M2
macrophages.
phenotypic
profile
cardiac
however,
much
more
diverse
should
not
be
reduced
these
subsets.
In
this
review,
we
describe
phenotypes
functions
macrophages
present
healthy,
well
infarcted
heart,
analyze
them
with
respect
polarization
states.
Furthermore,
discuss
therapeutic
strategies
utilize
macrophage
towards
anti-inflammatory
reparative
phenotype
for
treatment
Cells,
Journal Year:
2022,
Volume and Issue:
11(9), P. 1386 - 1386
Published: April 20, 2022
The
adult
mammalian
heart
contains
abundant
interstitial
and
perivascular
fibroblasts
that
expand
following
injury
play
a
reparative
role
but
also
contribute
to
maladaptive
fibrotic
remodeling.
Following
myocardial
infarction,
cardiac
undergo
dynamic
phenotypic
transitions,
contributing
the
regulation
of
inflammatory,
reparative,
angiogenic
responses.
This
review
manuscript
discusses
mechanisms
regulation,
roles
fate
in
infarcted
heart.
During
inflammatory
phase
infarct
healing,
release
alarmins
by
necrotic
cells
promotes
pro-inflammatory
matrix-degrading
fibroblast
phenotype
may
leukocyte
recruitment.
clearance
dead
matrix
debris
from
stimulates
anti-inflammatory
pathways
activates
transforming
growth
factor
(TGF)-β
cascades,
resulting
conversion
α-smooth
muscle
actin
(α-SMA)-expressing
myofibroblasts.
Activated
myofibroblasts
secrete
large
amounts
proteins
form
collagen-based
scar
protects
ventricle
catastrophic
complications,
such
as
rupture.
Moreover,
repair
stimulating
angiogenesis.
maturation,
disassemble
α-SMA+
stress
fibers
convert
specialized
serve
maintenance.
prolonged
activation
border
zone
remote
remodeling
myocardium
adverse
pathogenesis
failure.
In
addition
their
plasticity,
exhibit
remarkable
heterogeneity.
Subsets
with
distinct
profiles
be
responsible
for
wide
range
functions
populations
hearts.
International Journal of Molecular Sciences,
Journal Year:
2021,
Volume and Issue:
22(5), P. 2715 - 2715
Published: March 8, 2021
Cardiovascular
disease
is
the
leading
cause
of
mortality
and
morbidity
around
globe,
creating
a
substantial
socio-economic
burden
as
result.
Myocardial
infarction
significant
contributor
to
detrimental
impact
cardiovascular
disease.
The
death
cardiomyocytes
following
myocardial
causes
an
immune
response
which
leads
further
destruction
tissue,
subsequently,
results
in
formation
non-contractile
scar
tissue.
Macrophages
have
been
recognized
important
regulators
participants
inflammation
fibrosis
infarction.
are
generally
classified
into
two
distinct
groups,
namely,
classically
activated,
or
M1
macrophages,
alternatively
M2
macrophages.
phenotypic
profile
cardiac
however,
much
more
diverse
should
not
be
reduced
these
subsets.
In
this
review,
we
describe
phenotypes
functions
macrophages
present
healthy,
well
infarcted
heart,
analyze
them
with
respect
polarization
states.
Furthermore,
discuss
therapeutic
strategies
utilize
macrophage
towards
anti-inflammatory
reparative
phenotype
for
treatment
