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Further studies with neonatal cardiac regeneration mouse model suggested that major source of new
CMs is existing CMs, with the possibility of involvement of cardiac stem cells. In a vast majority of
cases, this condition ensues as the consequence of an acute (myocardial infarction) or chronic
ischaemic injury to the myocardium, followed by irreversible loss of cardiomyocytes (CMs), since
these cells are incapable of clinically significant replication in adult life. Figure 4:
Electrophysiological characterization of cardiomyocytes. This paradigm has been shaken by recent
works indicating that postnatal adult cardiomyocytes are able to re-enter in the cell cycle and
proliferate. This translates to nearly 160,000 deaths each year, an average of 435 people each day or
one death every three minutes. Our BHF Cardiovascular Regenerative Medicine Centre is currently
developing engineered heart tissue made from stem cell-derived cardiac muscle cells for grafting into
damaged hearts. These compounds were therefore re-evaluated under conditions that mimicked
reduced. By modulating retinoic acid signaling during hESC differentiation, we generated atrial-like
(hESC-atrial) and ventricular-like (hESC-ventricular) CMs. We found the expression of atrial-
specific ion channel genes, KCNA5 (encoding Kv1.5) and KCNJ3 (encoding Kir 3.1), in hESC-
atrial CMs and further demonstrated that these ion channel genes are regulated by COUP-TF
transcription factors. Constitutively active IK,ACh is predominantly observed in remodelled atria
from patients in permanent atrial fibrillation (AF). Using hiPSCs derived under chemically defined
conditions on synthetic matrices, we systematically developed an optimized cardiac differentiation
strategy, using a chemically defined medium consisting of just three components: the basal medium
RPMI 1640, L -ascorbic acid 2-phosphate and rice-derived recombinant human albumin. Nine
showed clear dose-dependence effects on field potential (FP) duration. Eleven reference compounds
were administrated to spontaneously beating clusters of cardiomyocytes from human pluripotent
stem cells (hPSC-CM) and the responses determined using multi-electrode arrays. Novel biomaterials
are being combined with the stem cells to produce an optimised functional cardiac patch. The cellular
and molecular mechanisms that control the regenerative capacity of the newt heart are unknown.
Newt cardiomyocytes implanted into regenerating limbs lost their cardiac phenotype and acquired
skeletal muscle or chondrocyte fates. Odegaard for analysis of teratoma slides, and K.R. Boheler and
R.L. Gundry for their insightful comments on this manuscript. This report is a review of studies
regarding generation of CM and pro. We have discovered new mechanisms underlying
chemotherapeutic cardiomyopathy and Takotsubo, or stress cardiomyopathy, and have identified a
cell signalling protein called MAP4K4 as a trigger for cardiac cell death. XEN-D0103 concentration-
dependently elevated the plateau potential. However, current preclinical studies carried out in non-
cardiac cell lines or animal models may not accurately represent the physiology of a human
cardiomyocyte (CM). See Full PDF Download PDF About Press Blog People Papers Topics Job
Board We're Hiring. You can download the paper by clicking the button above. Unexpectedly, two
potent blockers of the slow component of the delayed rectifier potassium current (I(Ks)), HMR1556
and JNJ303, had only minor effects on the extracellular FP of wild-type hPSC-CM despite evidence
of functional I(Ks) channels. This chemically defined platform for cardiac specification of hiPSCs
will allow the elucidation of cardiomyocyte macromolecular and metabolic requirements and will
provide a minimal system for the study of maturation and subtype specification. Figure 3:
Characterization of cardiomyocyte subtypes. Recent studies, however, have suggested that there is a
modest degree of cardiomyocyte (CM) turnover in adult mammalian heart, albeit not sufficient for
replacement of lost CMs following cardiac injuries. By understanding disease processes and
discovering new therapies we are endeavouring to revolutionise the treatment of heart diseases.
Moreover, in response to multiple ion channel blocker, vernakalant, and Kv1.5 blocker, XEN-D0101,
hESC-atrial but not hESC-ventricular CMs showed action potential (AP) prolongation due to a
reduction in early repolarization. Here we address this in a novel emerging assay system. Safety and
tolerability of XEN-D0103 were tested in a double-blind, randomised, placebo-controlled Phase-1
study.
You can download the paper by clicking the button above. Unexpectedly, two potent blockers of the
slow component of the delayed rectifier potassium current (I(Ks)), HMR1556 and JNJ303, had only
minor effects on the extracellular FP of wild-type hPSC-CM despite evidence of functional I(Ks)
channels. To investigate the effects of the highly selective Kv1.5 blocker XEN-D0103 on human
atrial action potentials (APs) at high excitation rates and to assess safety. The cellular and molecular
mechanisms that control the regenerative capacity of the newt heart are unknown. Newt
cardiomyocytes implanted into regenerating limbs lost their cardiac phenotype and acquired skeletal
muscle or chondrocyte fates. In this view, the understanding of main candidates regulating
cardiomyocyte cell cycle is of vital importance for future clinical approach. We use this knowledge
to guide improvements in diagnostic procedures, provide better clinical management and generate
novel treatments. In the current study, we tested whether human embryonic stem cell (hESC)-
derived atrial CMs could predict atrial selectivity of pharmacological compounds. We also use these
stem cell-derived human cardiac muscle cells as disease-in-a-dish models to understand the changes
induced by human genetic variants. Figure 2: Characterization and purification of cardiomyocytes
produced by chemically defined differentiation. Recent studies, however, have suggested that there
is a modest degree of cardiomyocyte (CM) turnover in adult mammalian heart, albeit not sufficient
for replacement of lost CMs following cardiac injuries. Nine showed clear dose-dependence effects
on field potential (FP) duration. Odegaard for analysis of teratoma slides, and K.R. Boheler and R.L.
Gundry for their insightful comments on this manuscript. Download citation Received: 15 October
2013 Accepted: 06 May 2014 Published: 15 June 2014 Issue Date: August 2014 DOI: Share this
article Anyone you share the following link with will be able to read this content: Get shareable link
Sorry, a shareable link is not currently available for this article. This chemically defined platform for
cardiac specification of hiPSCs will allow the elucidation of cardiomyocyte macromolecular and
metabolic requirements and will provide a minimal system for the study of maturation and subtype
specification. We have discovered new mechanisms underlying chemotherapeutic cardiomyopathy
and Takotsubo, or stress cardiomyopathy, and have identified a cell signalling protein called
MAP4K4 as a trigger for cardiac cell death. Reprogramming of cardiomyocytes depended on contact
with the limb blastema because cardiomyocytes implanted into intact, non-regenerating limbs or
cultured in vitro retained their original identity. By understanding disease processes and discovering
new therapies we are endeavouring to revolutionise the treatment of heart diseases. This report is a
review of studies regarding generation of CM and pro. However, current preclinical studies carried
out in non-cardiac cell lines or animal models may not accurately represent the physiology of a
human cardiomyocyte (CM). To browse Academia.edu and the wider internet faster and more
securely, please take a few seconds to upgrade your browser. Using hiPSCs derived under chemically
defined conditions on synthetic matrices, we systematically developed an optimized cardiac
differentiation strategy, using a chemically defined medium consisting of just three components: the
basal medium RPMI 1640, L -ascorbic acid 2-phosphate and rice-derived recombinant human
albumin. Figure 4: Electrophysiological characterization of cardiomyocytes. In a vast majority of
cases, this condition ensues as the consequence of an acute (myocardial infarction) or chronic
ischaemic injury to the myocardium, followed by irreversible loss of cardiomyocytes (CMs), since
these cells are incapable of clinically significant replication in adult life. These compounds were
therefore re-evaluated under conditions that mimicked reduced. Moreover, in response to multiple
ion channel blocker, vernakalant, and Kv1.5 blocker, XEN-D0101, hESC-atrial but not hESC-
ventricular CMs showed action potential (AP) prolongation due to a reduction in early
repolarization. Cardiac regeneration studies in various model organisms including zebrafish, newt,
and more recently in neonatal mouse, have demonstrated that CM dedifferentiation and concomitant
proliferation play important roles in replacement of lost CMs and restoration of cardiac contractility.
Figure 3: Characterization of cardiomyocyte subtypes. In particular, heart failure remains a
prominent cause of deaths, disability and financial costs, estimated to affect approximately 38
million people worldwide. Further studies with neonatal cardiac regeneration mouse model
suggested that major source of new CMs is existing CMs, with the possibility of involvement of
cardiac stem cells.
In SR and pAF preparations, the shortening effects on APD90 and ERP turned into prolongation at
high rates. Cardiac regeneration studies in various model organisms including zebrafish, newt, and
more recently in neonatal mouse, have demonstrated that CM dedifferentiation and concomitant
proliferation play important roles in replacement of lost CMs and restoration of cardiac contractility.
XEN-D0103 concentration-dependently elevated the plateau potential. Follow X, formerly known
as Twitter YouTube Instagram. This paradigm has been shaken by recent works indicating that
postnatal adult cardiomyocytes are able to re-enter in the cell cycle and proliferate. To browse
Academia.edu and the wider internet faster and more securely, please take a few seconds to upgrade
your browser. Download citation Received: 15 October 2013 Accepted: 06 May 2014 Published: 15
June 2014 Issue Date: August 2014 DOI: Share this article Anyone you share the following link with
will be able to read this content: Get shareable link Sorry, a shareable link is not currently available
for this article. In this view, the understanding of main candidates regulating cardiomyocyte cell
cycle is of vital importance for future clinical approach. Our BHF Cardiovascular Regenerative
Medicine Centre is currently developing engineered heart tissue made from stem cell-derived cardiac
muscle cells for grafting into damaged hearts. In particular, heart failure remains a prominent cause
of deaths, disability and financial costs, estimated to affect approximately 38 million people
worldwide. By understanding disease processes and discovering new therapies we are endeavouring
to revolutionise the treatment of heart diseases. Here we address this in a novel emerging assay
system. The cellular and molecular mechanisms that control the regenerative capacity of the newt
heart are unknown. Novel biomaterials are being combined with the stem cells to produce an
optimised functional cardiac patch. Numerous studies have now been conducted on induction of
cardiac regeneration and have identified various cardiogenic factors, cardiogenic micro ribonucleic
acid and cardiogenic small molecules. These compounds were therefore re-evaluated under
conditions that mimicked reduced. In the current study, we tested whether human embryonic stem
cell (hESC)-derived atrial CMs could predict atrial selectivity of pharmacological compounds.
Reprogramming of cardiomyocytes depended on contact with the limb blastema because
cardiomyocytes implanted into intact, non-regenerating limbs or cultured in vitro retained their
original identity. In a vast majority of cases, this condition ensues as the consequence of an acute
(myocardial infarction) or chronic ischaemic injury to the myocardium, followed by irreversible loss
of cardiomyocytes (CMs), since these cells are incapable of clinically significant replication in adult
life. Figure 2: Characterization and purification of cardiomyocytes produced by chemically defined
differentiation. We also use these stem cell-derived human cardiac muscle cells as disease-in-a-dish
models to understand the changes induced by human genetic variants. We use this knowledge to
guide improvements in diagnostic procedures, provide better clinical management and generate novel
treatments. Figure 3: Characterization of cardiomyocyte subtypes. Recent studies, however, have
suggested that there is a modest degree of cardiomyocyte (CM) turnover in adult mammalian heart,
albeit not sufficient for replacement of lost CMs following cardiac injuries. Here, we show that the
ability of newt cardiomyocytes to regenerate cardiac injuries correlates with their ability to
transdifferentiate into different cell types. To investigate the effects of the highly selective Kv1.5
blocker XEN-D0103 on human atrial action potentials (APs) at high excitation rates and to assess
safety. This report is a review of studies regarding generation of CM and pro. Newt cardiomyocytes
implanted into regenerating limbs lost their cardiac phenotype and acquired skeletal muscle or
chondrocyte fates. By modulating retinoic acid signaling during hESC differentiation, we generated
atrial-like (hESC-atrial) and ventricular-like (hESC-ventricular) CMs. We found the expression of
atrial-specific ion channel genes, KCNA5 (encoding Kv1.5) and KCNJ3 (encoding Kir 3.1), in
hESC-atrial CMs and further demonstrated that these ion channel genes are regulated by COUP-TF
transcription factors.
Using hiPSCs derived under chemically defined conditions on synthetic matrices, we systematically
developed an optimized cardiac differentiation strategy, using a chemically defined medium
consisting of just three components: the basal medium RPMI 1640, L -ascorbic acid 2-phosphate and
rice-derived recombinant human albumin. Recent studies, however, have suggested that there is a
modest degree of cardiomyocyte (CM) turnover in adult mammalian heart, albeit not sufficient for
replacement of lost CMs following cardiac injuries. To browse Academia.edu and the wider internet
faster and more securely, please take a few seconds to upgrade your browser. This paradigm has been
shaken by recent works indicating that postnatal adult cardiomyocytes are able to re-enter in the cell
cycle and proliferate. See Full PDF Download PDF About Press Blog People Papers Topics Job
Board We're Hiring. Novel biomaterials are being combined with the stem cells to produce an
optimised functional cardiac patch. By modulating retinoic acid signaling during hESC
differentiation, we generated atrial-like (hESC-atrial) and ventricular-like (hESC-ventricular) CMs.
We found the expression of atrial-specific ion channel genes, KCNA5 (encoding Kv1.5) and KCNJ3
(encoding Kir 3.1), in hESC-atrial CMs and further demonstrated that these ion channel genes are
regulated by COUP-TF transcription factors. This translates to nearly 160,000 deaths each year, an
average of 435 people each day or one death every three minutes. Here we address this in a novel
emerging assay system. However, current preclinical studies carried out in non-cardiac cell lines or
animal models may not accurately represent the physiology of a human cardiomyocyte (CM). We use
this knowledge to guide improvements in diagnostic procedures, provide better clinical management
and generate novel treatments. Reprogramming of cardiomyocytes depended on contact with the
limb blastema because cardiomyocytes implanted into intact, non-regenerating limbs or cultured in
vitro retained their original identity. Cardiac regeneration studies in various model organisms
including zebrafish, newt, and more recently in neonatal mouse, have demonstrated that CM
dedifferentiation and concomitant proliferation play important roles in replacement of lost CMs and
restoration of cardiac contractility. We also use these stem cell-derived human cardiac muscle cells as
disease-in-a-dish models to understand the changes induced by human genetic variants. Our BHF
Cardiovascular Regenerative Medicine Centre is currently developing engineered heart tissue made
from stem cell-derived cardiac muscle cells for grafting into damaged hearts. In SR and pAF
preparations, the shortening effects on APD90 and ERP turned into prolongation at high rates.
Further studies with neonatal cardiac regeneration mouse model suggested that major source of new
CMs is existing CMs, with the possibility of involvement of cardiac stem cells. Figure 2:
Characterization and purification of cardiomyocytes produced by chemically defined differentiation.
Figure 3: Characterization of cardiomyocyte subtypes. XEN-D0103 concentration-dependently
elevated the plateau potential. You can download the paper by clicking the button above. In this
view, the understanding of main candidates regulating cardiomyocyte cell cycle is of vital
importance for future clinical approach. This report is a review of studies regarding generation of
CM and pro. These compounds were therefore re-evaluated under conditions that mimicked reduced.
Eleven reference compounds were administrated to spontaneously beating clusters of
cardiomyocytes from human pluripotent stem cells (hPSC-CM) and the responses determined using
multi-electrode arrays. Figure 4: Electrophysiological characterization of cardiomyocytes. To
investigate the effects of the highly selective Kv1.5 blocker XEN-D0103 on human atrial action
potentials (APs) at high excitation rates and to assess safety. The cellular and molecular mechanisms
that control the regenerative capacity of the newt heart are unknown. You can download the paper by
clicking the button above. Unexpectedly, two potent blockers of the slow component of the delayed
rectifier potassium current (I(Ks)), HMR1556 and JNJ303, had only minor effects on the
extracellular FP of wild-type hPSC-CM despite evidence of functional I(Ks) channels.
This paradigm has been shaken by recent works indicating that postnatal adult cardiomyocytes are
able to re-enter in the cell cycle and proliferate. You can download the paper by clicking the button
above. Here we address this in a novel emerging assay system. Moreover, in response to multiple ion
channel blocker, vernakalant, and Kv1.5 blocker, XEN-D0101, hESC-atrial but not hESC-ventricular
CMs showed action potential (AP) prolongation due to a reduction in early repolarization. Figure 4:
Electrophysiological characterization of cardiomyocytes. We use this knowledge to guide
improvements in diagnostic procedures, provide better clinical management and generate novel
treatments. See Full PDF Download PDF About Press Blog People Papers Topics Job Board We're
Hiring. Constitutively active IK,ACh is predominantly observed in remodelled atria from patients in
permanent atrial fibrillation (AF). Our BHF Cardiovascular Regenerative Medicine Centre is
currently developing engineered heart tissue made from stem cell-derived cardiac muscle cells for
grafting into damaged hearts. Cardiac regeneration studies in various model organisms including
zebrafish, newt, and more recently in neonatal mouse, have demonstrated that CM dedifferentiation
and concomitant proliferation play important roles in replacement of lost CMs and restoration of
cardiac contractility. By understanding disease processes and discovering new therapies we are
endeavouring to revolutionise the treatment of heart diseases. To browse Academia.edu and the
wider internet faster and more securely, please take a few seconds to upgrade your browser. Recent
studies, however, have suggested that there is a modest degree of cardiomyocyte (CM) turnover in
adult mammalian heart, albeit not sufficient for replacement of lost CMs following cardiac injuries.
Odegaard for analysis of teratoma slides, and K.R. Boheler and R.L. Gundry for their insightful
comments on this manuscript. In particular, heart failure remains a prominent cause of deaths,
disability and financial costs, estimated to affect approximately 38 million people worldwide. In a
vast majority of cases, this condition ensues as the consequence of an acute (myocardial infarction)
or chronic ischaemic injury to the myocardium, followed by irreversible loss of cardiomyocytes
(CMs), since these cells are incapable of clinically significant replication in adult life. To browse
Academia.edu and the wider internet faster and more securely, please take a few seconds to upgrade
your browser. In SR and pAF preparations, the shortening effects on APD90 and ERP turned into
prolongation at high rates. Novel biomaterials are being combined with the stem cells to produce an
optimised functional cardiac patch. Figure 3: Characterization of cardiomyocyte subtypes. They have
strong cross-faculty interdisciplinary collaborations with Bioengineering, Computing, (notably
through the ElectroCardioMaths programme ), Physics (Photonics) and Materials. Download citation
Received: 15 October 2013 Accepted: 06 May 2014 Published: 15 June 2014 Issue Date: August
2014 DOI: Share this article Anyone you share the following link with will be able to read this
content: Get shareable link Sorry, a shareable link is not currently available for this article. This
chemically defined platform for cardiac specification of hiPSCs will allow the elucidation of
cardiomyocyte macromolecular and metabolic requirements and will provide a minimal system for
the study of maturation and subtype specification. This report is a review of studies regarding
generation of CM and pro. Newt cardiomyocytes implanted into regenerating limbs lost their cardiac
phenotype and acquired skeletal muscle or chondrocyte fates. You can download the paper by
clicking the button above. We also use these stem cell-derived human cardiac muscle cells as disease-
in-a-dish models to understand the changes induced by human genetic variants. Further studies with
neonatal cardiac regeneration mouse model suggested that major source of new CMs is existing
CMs, with the possibility of involvement of cardiac stem cells. In this view, the understanding of
main candidates regulating cardiomyocyte cell cycle is of vital importance for future clinical
approach.
To investigate the effects of the highly selective Kv1.5 blocker XEN-D0103 on human atrial action
potentials (APs) at high excitation rates and to assess safety. Nine showed clear dose-dependence
effects on field potential (FP) duration. Here, we show that the ability of newt cardiomyocytes to
regenerate cardiac injuries correlates with their ability to transdifferentiate into different cell types.
Figure 2: Characterization and purification of cardiomyocytes produced by chemically defined
differentiation. Unexpectedly, two potent blockers of the slow component of the delayed rectifier
potassium current (I(Ks)), HMR1556 and JNJ303, had only minor effects on the extracellular FP of
wild-type hPSC-CM despite evidence of functional I(Ks) channels. Safety and tolerability of XEN-
D0103 were tested in a double-blind, randomised, placebo-controlled Phase-1 study. Odegaard for
analysis of teratoma slides, and K.R. Boheler and R.L. Gundry for their insightful comments on this
manuscript. However, current preclinical studies carried out in non-cardiac cell lines or animal
models may not accurately represent the physiology of a human cardiomyocyte (CM). This
chemically defined platform for cardiac specification of hiPSCs will allow the elucidation of
cardiomyocyte macromolecular and metabolic requirements and will provide a minimal system for
the study of maturation and subtype specification. This report is a review of studies regarding
generation of CM and pro. Here we address this in a novel emerging assay system. In SR and pAF
preparations, the shortening effects on APD90 and ERP turned into prolongation at high rates.
Download citation Received: 15 October 2013 Accepted: 06 May 2014 Published: 15 June 2014
Issue Date: August 2014 DOI: Share this article Anyone you share the following link with will be
able to read this content: Get shareable link Sorry, a shareable link is not currently available for this
article. By modulating retinoic acid signaling during hESC differentiation, we generated atrial-like
(hESC-atrial) and ventricular-like (hESC-ventricular) CMs. We found the expression of atrial-
specific ion channel genes, KCNA5 (encoding Kv1.5) and KCNJ3 (encoding Kir 3.1), in hESC-
atrial CMs and further demonstrated that these ion channel genes are regulated by COUP-TF
transcription factors. See Full PDF Download PDF About Press Blog People Papers Topics Job
Board We're Hiring. Recent studies, however, have suggested that there is a modest degree of
cardiomyocyte (CM) turnover in adult mammalian heart, albeit not sufficient for replacement of lost
CMs following cardiac injuries. We use this knowledge to guide improvements in diagnostic
procedures, provide better clinical management and generate novel treatments. Numerous studies
have now been conducted on induction of cardiac regeneration and have identified various
cardiogenic factors, cardiogenic micro ribonucleic acid and cardiogenic small molecules. In a vast
majority of cases, this condition ensues as the consequence of an acute (myocardial infarction) or
chronic ischaemic injury to the myocardium, followed by irreversible loss of cardiomyocytes (CMs),
since these cells are incapable of clinically significant replication in adult life. Newt cardiomyocytes
implanted into regenerating limbs lost their cardiac phenotype and acquired skeletal muscle or
chondrocyte fates. This translates to nearly 160,000 deaths each year, an average of 435 people each
day or one death every three minutes. You can download the paper by clicking the button above.
Further studies with neonatal cardiac regeneration mouse model suggested that major source of new
CMs is existing CMs, with the possibility of involvement of cardiac stem cells. In particular, heart
failure remains a prominent cause of deaths, disability and financial costs, estimated to affect
approximately 38 million people worldwide. Using hiPSCs derived under chemically defined
conditions on synthetic matrices, we systematically developed an optimized cardiac differentiation
strategy, using a chemically defined medium consisting of just three components: the basal medium
RPMI 1640, L -ascorbic acid 2-phosphate and rice-derived recombinant human albumin.
Constitutively active IK,ACh is predominantly observed in remodelled atria from patients in
permanent atrial fibrillation (AF). By understanding disease processes and discovering new therapies
we are endeavouring to revolutionise the treatment of heart diseases. XEN-D0103 concentration-
dependently elevated the plateau potential. Cardiac regeneration studies in various model organisms
including zebrafish, newt, and more recently in neonatal mouse, have demonstrated that CM
dedifferentiation and concomitant proliferation play important roles in replacement of lost CMs and
restoration of cardiac contractility.