Jeffery D. Molkentin

Redefining the roles of p38 and JNK signaling in cardiac hypertrophy: dichotomy between cultured myocytes and animal models.

Genetic loss of calcineurin blocks mechanical overload-induced skeletal muscle fiber type switching but not hypertrophy.

Calcineurin-NFAT signaling regulates the cardiac hypertrophic response in coordination with the MAPKs.

Calcium-calcineurin signaling in the regulation of cardiac hypertrophy.

Cardiomyocytes fuse with surrounding noncardiomyocytes and reenter the cell cycle.

STRESS signaling pathways that modulate cardiac myocyte apoptosis.

Identification of a cooperative mechanism involving interleukin-13 and eotaxin-2 in experimental allergic lung inflammation.

Direct and indirect interactions between calcineurin-NFAT and MEK1-extracellular signal-regulated kinase 1/2 signaling pathways regulate cardiac gene expression and cellular growth.

Regulation of calcineurin through transcriptional induction of the calcineurin A beta promoter in vitro and in vivo.

Inhibition of p38 reduces myocardial infarction injury in the mouse but not pig after ischemia-reperfusion.

The DnaJ-related factor Mrj interacts with nuclear factor of activated T cells c3 and mediates transcriptional repression through class II histone deacetylase recruitment.

Myocyte enhancer factors 2A and 2C induce dilated cardiomyopathy in transgenic mice.

Dichotomy of Ca2+ in the heart: contraction versus intracellular signaling.

Modulatory calcineurin-interacting proteins 1 and 2 function as calcineurin facilitators in vivo.

Direct interaction and reciprocal regulation between ASK1 and calcineurin-NFAT control cardiomyocyte death and growth.

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

Calcineurin-dependent cardiomyopathy is activated by TRPC in the adult mouse heart.

Pharmacological- and gene therapy-based inhibition of protein kinase Calpha/beta enhances cardiac contractility and attenuates heart failure.

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

Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death.

Mediating ERK 1/2 signaling rescues congenital heart defects in a mouse model of Noonan syndrome.

Ca2+- and mitochondrial-dependent cardiomyocyte necrosis as a primary mediator of heart failure.

Genetic inhibition of cardiac ERK1/2 promotes stress-induced apoptosis and heart failure but has no effect on hypertrophy in vivo.

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.

Does contractile Ca2+ control calcineurin-NFAT signaling and pathological hypertrophy in cardiac myocytes?

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

Ca2+ influx through T- and L-type Ca2+ channels have different effects on myocyte contractility and induce unique cardiac phenotypes.

With great power comes great responsibility: using mouse genetics to study cardiac hypertrophy and failure.

Role of ERK1/2 signaling in congenital valve malformations in Noonan syndrome.

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

Rcan1 negatively regulates Fc epsilonRI-mediated signaling and mast cell function.

Interaction between TAK1-TAB1-TAB2 and RCAN1-calcineurin defines a signalling nodal control point.

PKCalpha regulates platelet granule secretion and thrombus formation in mice.

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

The mitochondrial permeability transition pore in motor neurons: involvement in the pathobiology of ALS mice.

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

Adenine nucleotide translocase-1 induces cardiomyocyte death through upregulation of the pro-apoptotic protein Bax.

Periostin as a heterofunctional regulator of cardiac development and disease.

Protein kinase C{alpha}, but not PKC{beta} or PKC{gamma}, regulates contractility and heart failure susceptibility: implications for ruboxistaurin as a novel therapeutic approach.

CaMKII negatively regulates calcineurin-NFAT signaling in cardiac myocytes.

Lack of periostin leads to suppression of Notch1 signaling and calcific aortic valve disease.

Cdc42 is an antihypertrophic molecular switch in the mouse heart.

ASK1 regulates cardiomyocyte death but not hypertrophy in transgenic mice.

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

Blockade of Hsp20 phosphorylation exacerbates cardiac ischemia/reperfusion injury by suppressed autophagy and increased cell death.

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

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

alpha1G-dependent T-type Ca2+ current antagonizes cardiac hypertrophy through a NOS3-dependent mechanism in mice.

Heart-specific deletion of CnB1 reveals multiple mechanisms whereby calcineurin regulates cardiac growth and function.

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

Extracellular signal-regulated kinase 1/2 (ERK1/2) signaling in cardiac hypertrophy.

TRPC channels are necessary mediators of pathologic cardiac hypertrophy.

Apoptotic cell death "Nixed" by an ER-mitochondrial necrotic pathway.

Functional divergence of platelet protein kinase C (PKC) isoforms in thrombus formation on collagen.

Enhanced basal contractility but reduced excitation-contraction coupling efficiency and beta-adrenergic reserve of hearts with increased Cav1.2 activity.

Proteasome functional insufficiency activates the calcineurin-NFAT pathway in cardiomyocytes and promotes maladaptive remodelling of stressed mouse hearts.

The IP3 receptor regulates cardiac hypertrophy in response to select stimuli.

Debio-025 is more effective than prednisone in reducing muscular pathology in mdx mice.

CIB1 is a regulator of pathological cardiac hypertrophy.

The transcription factor GATA-6 regulates pathological cardiac hypertrophy.

The role of calcium/calmodulin-activated calcineurin in rapid and slow endocytosis at central synapses.

Research priorities in hypertrophic cardiomyopathy: report of a Working Group of the National Heart, Lung, and Blood Institute.

Cyclophilin D controls mitochondrial pore-dependent Ca(2+) exchange, metabolic flexibility, and propensity for heart failure in mice.

Magnetic resonance imaging assessment of cardiac dysfunction in δ-sarcoglycan null mice.

Protein kinase Cα as a heart failure therapeutic target.

Monophosphothreonyl extracellular signal-regulated kinases 1 and 2 (ERK1/2) are formed endogenously in intact cardiac myocytes and are enzymically active.

Calcium influx through Cav1.2 is a proximal signal for pathological cardiomyocyte hypertrophy.

GATA6 promotes angiogenic function and survival in endothelial cells by suppression of autocrine transforming growth factor beta/activin receptor-like kinase 5 signaling.

Extracellular signal-regulated kinases 1 and 2 regulate the balance between eccentric and concentric cardiac growth.

Molecular pathways underlying cardiac remodeling during pathophysiological stimulation.

TRPC channels as effectors of cardiac hypertrophy.

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

The transcription factor C/EBPbeta serves as a master regulator of physiologic cardiac hypertrophy.

Moderate calcium channel dysfunction in adult mice with inducible cardiomyocyte-specific excision of the cacnb2 gene.

Mechanisms of necroptosis in T cells.

Dysfunctional ryanodine receptor and cardiac hypertrophy: role of signaling molecules.

Myostatin from the heart: local and systemic actions in cardiac failure and muscle wasting.

Modulation of chromatin position and gene expression by HDAC4 interaction with nucleoporins.

A critical function for Ser-282 in cardiac Myosin binding protein-C phosphorylation and cardiac function.

Unraveling the secrets of a double life: contractile versus signaling Ca2+ in a cardiac myocyte.

Regulation of angiogenesis by a non-canonical Wnt-Flt1 pathway in myeloid cells.

Placental growth factor regulates cardiac adaptation and hypertrophy through a paracrine mechanism.

Tinman/Nkx2-5 acts via miR-1 and upstream of Cdc42 to regulate heart function across species.

Serine 105 phosphorylation of transcription factor GATA4 is necessary for stress-induced cardiac hypertrophy in vivo.

RhoA protects the mouse heart against ischemia/reperfusion injury.

The permeability transition pore controls cardiac mitochondrial maturation and myocyte differentiation.

Inhibition of PKCα/β with ruboxistaurin antagonizes heart failure in pigs after myocardial infarction injury.

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

Pharmacological and genetic inhibition of calcineurin protects against carbachol-induced pathological zymogen activation and acinar cell injury.

Interaction between NFκB and NFAT coordinates cardiac hypertrophy and pathological remodeling.

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

Placental growth factor as a protective paracrine effector in the heart.

Constitutively active MEK1 rescues cardiac dysfunction caused by overexpressed GSK-3α during aging and hemodynamic pressure overload.

Lost in transgenesis: a user's guide for genetically manipulating the mouse in cardiac research.

Sarcolipin is a newly identified regulator of muscle-based thermogenesis in mammals.

Unrestrained p38 MAPK activation in Dusp1/4 double-null mice induces cardiomyopathy.

A TRPC6-dependent pathway for myofibroblast transdifferentiation and wound healing in vivo.

Is p53 the long-sought molecular trigger for cyclophilin D-regulated mitochondrial permeability transition pore formation and necrosis?

Bile acids induce pancreatic acinar cell injury and pancreatitis by activating calcineurin.

Mutual antagonism between IP(3)RII and miRNA-133a regulates calcium signals and cardiac hypertrophy.

Molecular basis of physiological heart growth: fundamental concepts and new players.

Signaling effectors underlying pathologic growth and remodeling of the heart.

Physiologic functions of cyclophilin D and the mitochondrial permeability transition pore.

CaMKII does it again: even the mitochondria cannot escape its influence.

Parsing good versus bad signaling pathways in the heart: role of calcineurin-nuclear factor of activated T-cells.

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

Differential expression of embryonic epicardial progenitor markers and localization of cardiac fibrosis in adult ischemic injury and hypertensive heart disease.

Myofibroblasts: trust your heart and let fate decide.

Overexpression of the Na+/K+ ATPase α2 but not α1 isoform attenuates pathological cardiac hypertrophy and remodeling.

Apoptosis repressor with a CARD domain (ARC) restrains Bax-mediated pathogenesis in dystrophic skeletal muscle.

Parsing the roles of the transcription factors GATA-4 and GATA-6 in the adult cardiac hypertrophic response.

Response to Torella et al.

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

Genetic manipulation of the cardiac mitochondrial phosphate carrier does not affect permeability transition.

c-kit+ cells minimally contribute cardiomyocytes to the heart.

Repression of cyclin D1 expression is necessary for the maintenance of cell cycle exit in adult mammalian cardiomyocytes.

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

Identifying the components of the elusive mitochondrial permeability transition pore.

Transient receptor potential channels contribute to pathological structural and functional remodeling after myocardial infarction.

Excess SMAD signaling contributes to heart and muscle dysfunction in muscular dystrophy.

Sumo E2 enzyme UBC9 is required for efficient protein quality control in cardiomyocytes.

Myofiber-specific inhibition of TGFβ signaling protects skeletal muscle from injury and dystrophic disease in mice.

Letter by Molkentin regarding article, "The absence of evidence is not evidence of absence: the pitfalls of Cre Knock-Ins in the c-Kit Locus".

Transforming growth factor β-activated kinase 1 signaling pathway critically regulates myocardial survival and remodeling.

The β isoform of the catalytic subunit of protein phosphatase 2B restrains platelet function by suppressing outside-in αII b β3 integrin signaling.

RhoA signaling in cardiomyocytes protects against stress-induced heart failure but facilitates cardiac fibrosis.

Targeting latent TGFβ release in muscular dystrophy.

An emerging consensus on cardiac regeneration.

Physiological and pathological roles of the mitochondrial permeability transition pore in the heart.

SERCA1 overexpression minimizes skeletal muscle damage in dystrophic mouse models.

Sarcolipin overexpression improves muscle energetics and reduces fatigue.

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

Exposure to Radiocontrast Agents Induces Pancreatic Inflammation by Activation of Nuclear Factor-κB, Calcium Signaling, and Calcineurin.

Regulated necrotic cell death: the passive aggressive side of Bax and Bak.

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.

Calcineurin Links Mitochondrial Elongation with Energy Metabolism.

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

TAK1 Regulates Myocardial Response to Pathological Stress via NFAT, NFκB, and Bnip3 Pathways.

Deletion of Periostin Protects Against Atherosclerosis in Mice by Altering Inflammation and Extracellular Matrix Remodeling.

Persistent increases in Ca(2+) influx through Cav1.2 shortens action potential and causes Ca(2+) overload-induced afterdepolarizations and arrhythmias.

MBNL1-mediated regulation of differentiation RNAs promotes myofibroblast transformation and the fibrotic response.

Individual Cardiac Mitochondria Undergo Rare Transient Permeability Transition Pore Openings.

Genetic overexpression of Serpina3n attenuates muscular dystrophy in mice.

Most of the Dust Has Settled: cKit+ Progenitor Cells Are an Irrelevant Source of Cardiac Myocytes In Vivo.

Cyclophilin D regulates necrosis, but not apoptosis, of murine eosinophils.

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

A Tension-Based Model Distinguishes Hypertrophic versus Dilated Cardiomyopathy.

DUSP8 Regulates Cardiac Ventricular Remodeling by Altering ERK1/2 Signaling.

Genetic lineage tracing defines myofibroblast origin and function in the injured heart.

Inositol 1,4,5-trisphosphate-mediated sarcoplasmic reticulum-mitochondrial crosstalk influences adenosine triphosphate production via mitochondrial Ca2+ uptake through the mitochondrial ryanodine receptor in cardiac myocytes.

Regulation of cardiac hypertrophy and remodeling through the dual-specificity MAPK phosphatases (DUSPs).

Thrombospondin 1 protects pancreatic β-cells from lipotoxicity via the PERK-NRF2 pathway.

Thrombospondin expression in myofibers stabilizes muscle membranes.

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

RCANs regulate the convergent roles of NFATc1 in bone homeostasis.

The Elusive Progenitor Cell in Cardiac Regeneration: Slip Slidin' Away.

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.

Redefining the identity of cardiac fibroblasts.

The mitochondrial Na/Ca exchanger is essential for Ca homeostasis and viability.

Preexisting endothelial cells mediate cardiac neovascularization after injury.

An Unbiased High-Throughput Screen to Identify Novel Effectors That Impact on Cardiomyocyte Aggregate Levels.

Cardiomyocyte Regeneration: A Consensus Statement.

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.

Fibroblast-specific TGF-β-Smad2/3 signaling underlies cardiac fibrosis.

Spatial Gene Profiling in the Ischemic Heart: Fibroblasts Put on Their SOX.

Identity Crisis for Regenerative Cardiac cKit Cells.

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

BEX1 is an RNA-dependent mediator of cardiomyopathy.

Increasing T-type calcium channel activity by β-adrenergic stimulation contributes to β-adrenergic regulation of heart rates.

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Genetic Reduction in Left Ventricular Protein Kinase C-α and Adverse Ventricular Remodeling in Human Subjects.

van Berlo et al. reply.

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.

Gata4-Dependent Differentiation of c-Kit Derived Endothelial Cells Underlies Artefactual Cardiomyocyte Regeneration in the Heart.

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

Developmental vascular regression is regulated by a Wnt/β-catenin, MYC and CDKN1A pathway that controls cell proliferation and cell death.

New Myocyte Formation in the Adult Heart: Endogenous Sources and Therapeutic Implications.

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

Protein Kinase C Inhibition With Ruboxistaurin Increases Contractility and Reduces Heart Size in a Swine Model of Heart Failure With Reduced Ejection Fraction.

Applying Modern Transcriptomics to Interrogate the Human Cardiac Fibroblast.

Nuclear calcineurin is a sensor for detecting Ca release from the nuclear envelope via IPR.

Undeniable Evidence That the Adult Mammalian Heart Lacks an Endogenous Regenerative Stem Cell.

The mitochondrial calcium uniporter underlies metabolic fuel preference in skeletal muscle.

Evidence for Minimal Cardiogenic Potential of Stem Cell Antigen 1-Positive Cells in the Adult Mouse Heart.

Cardiac-specific deficiency of the mitochondrial calcium uniporter augments fatty acid oxidation and functional reserve.

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

Overlapping and differential functions of ATF6α versus ATF6β in the mouse heart.

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.

Cell-specific ablation of Hsp47 defines the collagen-producing cells in the injured heart

The EYA3 tyrosine phosphatase activity promotes pulmonary vascular remodeling in pulmonary arterial hypertension.

CARdiac Immunotherapy: T Cells Engineered to Treat the Fibrotic Heart.

Hippo signaling does it again: arbitrating cardiac fibroblast identity and activation.

A novel class of cardioprotective small-molecule PTP inhibitors.

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

MEF2C repressor variant deregulation leads to cell cycle re-entry and development of heart failure.

Cysteine 202 of cyclophilin D is a site of multiple post-translational modifications and plays a role in cardioprotection.

Hyperglycemia Acutely Increases Cytosolic Reactive Oxygen Species via -linked GlcNAcylation and CaMKII Activation in Mouse Ventricular Myocytes.

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

MCUb Induction Protects the Heart From Postischemic Remodeling.

A 20/20 view of ANT function in mitochondrial biology and necrotic cell death.

Type 2 diabetes risk gene Dusp8 regulates hypothalamic Jnk signaling and insulin sensitivity.

A specialized population of Periostin-expressing cardiac fibroblasts contributes to postnatal cardiomyocyte maturation and innervation.

Ontogeny of arterial macrophages defines their functions in homeostasis and inflammation.

Interleukin-1α dependent survival of cardiac fibroblasts is associated with StAR/STARD1 expression and improved cardiac remodeling and function after myocardial infarction.

Resident macrophages keep mitochondria running in the heart.