Michelle Sargent

Age-dependent effect of myostatin blockade on disease severity in a murine model of limb-girdle muscular dystrophy.

Cardiac myosin binding protein C phosphorylation is cardioprotective.

Genetic disruption of calcineurin improves skeletal muscle pathology and cardiac disease in a mouse model of limb-girdle muscular dystrophy.

Inducible and myocyte-specific inhibition of PKCalpha enhances cardiac contractility and protects against infarction-induced heart failure.

Cardiomyocyte GATA4 functions as a stress-responsive regulator of angiogenesis in the murine heart.

Genetic and pharmacologic inhibition of mitochondrial-dependent necrosis attenuates muscular dystrophy.

DUSP6 (MKP3) null mice show enhanced ERK1/2 phosphorylation at baseline and increased myocyte proliferation in the heart affecting disease susceptibility.

Genetic manipulation of periostin expression in the heart does not affect myocyte content, cell cycle activity, or cardiac repair.

Cardiac myosin binding protein-C phosphorylation in a {beta}-myosin heavy chain background.

Plasma membrane Ca2+-ATPase isoform 4 antagonizes cardiac hypertrophy in association with calcineurin inhibition in rodents.

ASK1 regulates cardiomyocyte death but not hypertrophy in transgenic mice.

Genetic manipulation of dysferlin expression in skeletal muscle: novel insights into muscular dystrophy.

Calcineurin protects the heart in a murine model of dilated cardiomyopathy.

Calcium influx is sufficient to induce muscular dystrophy through a TRPC-dependent mechanism.

Genetic deletion of myostatin from the heart prevents skeletal muscle atrophy in heart failure.

Mitigation of muscular dystrophy in mice by SERCA overexpression in skeletal muscle.

Decreased cardiac L-type Ca²⁺ channel activity induces hypertrophy and heart failure in mice.

A thrombospondin-dependent pathway for a protective ER stress response.

Bax and Bak function as the outer membrane component of the mitochondrial permeability pore in regulating necrotic cell death in mice.

Enhanced Ca²⁺ influx from STIM1-Orai1 induces muscle pathology in mouse models of muscular dystrophy.

P38α MAPK underlies muscular dystrophy and myofiber death through a Bax-dependent mechanism.

Genetic Analysis of Connective Tissue Growth Factor as an Effector of Transforming Growth Factor β Signaling and Cardiac Remodeling.

Necroptosis Interfaces with MOMP and the MPTP in Mediating Cell Death.

The Mitochondrial Calcium Uniporter Selectively Matches Metabolic Output to Acute Contractile Stress in the Heart.

STIM1 elevation in the heart results in aberrant Ca²⁺ handling and cardiomyopathy.

Cardiac-specific deletion of protein phosphatase 1β promotes increased myofilament protein phosphorylation and contractile alterations.

Dissection of Thrombospondin-4 Domains Involved in Intracellular Adaptive Endoplasmic Reticulum Stress-Responsive Signaling.

Genetic overexpression of Serpina3n attenuates muscular dystrophy in mice.

Cathepsin S Contributes to the Pathogenesis of Muscular Dystrophy in Mice.

Thrombospondin expression in myofibers stabilizes muscle membranes.

Nemo-Like Kinase (NLK) Is a Pathological Signaling Effector in the Mouse Heart.

Fibroblast-Specific Genetic Manipulation of p38 Mitogen-Activated Protein Kinase In Vivo Reveals Its Central Regulatory Role in Fibrosis.

Caveolae-localized L-type Ca2+ channels do not contribute to function or hypertrophic signalling in the mouse heart.

Mitsugumin 29 regulates t-tubule architecture in the failing heart.

TGFBI functions similar to periostin but is uniquely dispensable during cardiac injury.

Pharmacological and Activated Fibroblast Targeting of Gβγ-GRK2 After Myocardial Ischemia Attenuates Heart Failure Progression.

Autophagic cell death is dependent on lysosomal membrane permeability through Bax and Bak.

Inhibiting Fibronectin Attenuates Fibrosis and Improves Cardiac Function in a Model of Heart Failure.

Specialized fibroblast differentiated states underlie scar formation in the infarcted mouse heart.

Defective Flux of Thrombospondin-4 through the Secretory Pathway Impairs Cardiomyocyte Membrane Stability and Causes Cardiomyopathy.

Genetic Lineage Tracing of Sca-1 Cells Reveals Endothelial but Not Myogenic Contribution to the Murine Heart.

Thrombospondin-3 augments injury-induced cardiomyopathy by intracellular integrin inhibition and sarcolemmal instability.

ERK1/2 signaling induces skeletal muscle slow fiber-type switching and reduces muscular dystrophy disease severity.

Disruption of valosin-containing protein activity causes cardiomyopathy and reveals pleiotropic functions in cardiac homeostasis.

An acute immune response underlies the benefit of cardiac stem cell therapy.

Cardiac Cell Therapy Rejuvenates the Infarcted Rodent Heart via Direct Injection but Not by Vascular Infusion.

MCUb Induction Protects the Heart From Postischemic Remodeling.