Ronglih Liao

Phenotypic spectrum caused by transgenic overexpression of activated Akt in the heart.

Heterozygous cellular glutathione peroxidase deficiency in the mouse: abnormalities in vascular and cardiac function and structure.

Cardiac-specific overexpression of GLUT1 prevents the development of heart failure attributable to pressure overload in mice.

Influence of gender on the response to hemodynamic overload after myocardial infarction.

Titin determines the Frank-Starling relation in early diastole.

Mg-ATPase and Ca+ activated myosin AtPase activity in ventricular myofibrils from non-failing and diseased human hearts--effects of calcium sensitizing agents MCI-154, DPI 201-106, and caffeine.

Deletion of cytosolic phospholipase A2 promotes striated muscle growth.

Glucose-6-phosphate dehydrogenase modulates cytosolic redox status and contractile phenotype in adult cardiomyocytes.

Myocyte contractile activity modulates norepinephrine cytotoxicity and survival effects of neuregulin-1beta.

Anthracyclines induce calpain-dependent titin proteolysis and necrosis in cardiomyocytes.

Increased myocardial dysfunction after ischemia-reperfusion in mice lacking glucose-6-phosphate dehydrogenase.

Pressure overload-induced myocardial hypertrophy in mice does not require gp91phox.

Glycogen synthase kinase-3beta regulates growth, calcium homeostasis, and diastolic function in the heart.

Human amyloidogenic light chains directly impair cardiomyocyte function through an increase in cellular oxidant stress.

Gene transfer of parvalbumin improves diastolic dysfunction in senescent myocytes.

Cardiac endothelial cells regulate reactive oxygen species-induced cardiomyocyte apoptosis through neuregulin-1beta/erbB4 signaling.

Mineralocorticoid receptor inhibition ameliorates the transition to myocardial failure and decreases oxidative stress and inflammation in mice with chronic pressure overload.

Akt3 overexpression in the heart results in progression from adaptive to maladaptive hypertrophy.

Alpha-adrenergic receptor-stimulated hypertrophy in adult rat ventricular myocytes is mediated via thioredoxin-1-sensitive oxidative modification of thiols on Ras.

Mesenchymal stem cells in the infarcted heart.

Genetic determinants of vascular oxidant stress and endothelial dysfunction.

Yin and Yang of myocardial transforming growth factor-beta1: timing is everything.

CD31- but Not CD31+ cardiac side population cells exhibit functional cardiomyogenic differentiation.

Disruption of coordinated cardiac hypertrophy and angiogenesis contributes to the transition to heart failure.

Restoration of cardiac progenitor cells after myocardial infarction by self-proliferation and selective homing of bone marrow-derived stem cells.

Selective loss of fine tuning of Gq/11 signaling by RGS2 protein exacerbates cardiomyocyte hypertrophy.

Regulation of vascular endothelial growth factor expression and vascularization in the myocardium by insulin receptor and PI3K/Akt pathways in insulin resistance and ischemia.

Transcription factor CHF1/Hey2 suppresses cardiac hypertrophy through an inhibitory interaction with GATA4.

The beta-catenin/T-cell factor/lymphocyte enhancer factor signaling pathway is required for normal and stress-induced cardiac hypertrophy.

PICOT inhibits cardiac hypertrophy and enhances ventricular function and cardiomyocyte contractility.

A novel microfluidic impedance assay for monitoring endothelin-induced cardiomyocyte hypertrophy.

Collagen-GAG scaffolds grafted onto myocardial infarcts in a rat model: a delivery vehicle for mesenchymal stem cells.

Delayed erythropoietin therapy reduces post-MI cardiac remodeling only at a dose that mobilizes endothelial progenitor cells.

Cardiomyocyte-specific overexpression of nitric oxide synthase 3 prevents myocardial dysfunction in murine models of septic shock.

Essential role of insulin and insulin-like growth factor 1 receptor signaling in cardiac development and function.

Aldosterone impairs vascular reactivity by decreasing glucose-6-phosphate dehydrogenase activity.

Peroxisome proliferator-activated receptor alpha-independent actions of fenofibrate exacerbates left ventricular dilation and fibrosis in chronic pressure overload.

Cell therapy in heart failure.

Kruppel-like factor 15 is a regulator of cardiomyocyte hypertrophy.

Adult stem cells and heart regeneration.

Simultaneous orientation and cellular force measurements in adult cardiac myocytes using three-dimensional polymeric microstructures.

The bone marrow--cardiac axis of myocardial regeneration.

Long-term effects of increased glucose entry on mouse hearts during normal aging and ischemic stress.

Not all hypertrophy is created equal.

Parasympathetic response in chick myocytes and mouse heart is controlled by SREBP.

Enhanced calcium cycling and contractile function in transgenic hearts expressing constitutively active G alpha o* protein.

A novel mutant cardiac troponin C disrupts molecular motions critical for calcium binding affinity and cardiomyocyte contractility.

Real-time monitoring primary cardiomyocyte adhesion based on electrochemical impedance spectroscopy and electrical cell-substrate impedance sensing.

Isolation, culture, and functional analysis of adult mouse cardiomyocytes.

Deletion of Ptpn11 (Shp2) in cardiomyocytes causes dilated cardiomyopathy via effects on the extracellular signal-regulated kinase/mitogen-activated protein kinase and RhoA signaling pathways.

Pump to survive: novel cytoprotective strategies for cardiac progenitor cells.

Evolving cell-based therapies for heart failure patients.

Role of the ATP-binding cassette transporter Abcg2 in the phenotype and function of cardiac side population cells.

Disruption of striated preferentially expressed gene locus leads to dilated cardiomyopathy in mice.

Impedance-based monitoring of ongoing cardiomyocyte death induced by tumor necrosis factor-alpha.

A novel role for tumor necrosis factor-like weak inducer of apoptosis (TWEAK) in the development of cardiac dysfunction and failure.

Role of SREBP-1 in the development of parasympathetic dysfunction in the hearts of type 1 diabetic Akita mice.

Increased glucose uptake and oxidation in mouse hearts prevent high fatty acid oxidation but cause cardiac dysfunction in diet-induced obesity.

Intervention of cardiomyocyte death based on real-time monitoring of cell adhesion through impedance sensing.

Loss of cardiac microRNA-mediated regulation leads to dilated cardiomyopathy and heart failure.

A feedback loop involving the Phd3 prolyl hydroxylase tunes the mammalian hypoxic response in vivo.

Regulation of VASP phosphorylation in cardiac myocytes: differential regulation by cyclic nucleotides and modulation of protein expression in diabetic and hypertrophic heart.

Glutathione peroxidase deficiency exacerbates ischemia-reperfusion injury in male but not female myocardium: insights into antioxidant compensatory mechanisms.

Intervention of cardiomyocyte death based on the impedance-sensing technique of monitoring cell adhesion.

CHF1/Hey2 promotes physiological hypertrophy in response to pressure overload through selective repression and activation of specific transcriptional pathways.

Effects of trimetazidine, a partial inhibitor of fatty acid oxidation, on ventricular function and survival after myocardial infarction and reperfusion in the rat.

Redox-mediated reciprocal regulation of SERCA and Na+-Ca2+ exchanger contributes to sarcoplasmic reticulum Ca2+ depletion in cardiac myocytes.

Amyloidogenic light chains induce cardiomyocyte contractile dysfunction and apoptosis via a non-canonical p38alpha MAPK pathway.

Inhibition of notch1-dependent cardiomyogenesis leads to a dilated myopathy in the neonatal heart.

The paradoxical role of inflammation in cardiac repair and regeneration.

Isolation of resident cardiac progenitor cells by Hoechst 33342 staining.

Loss of hypoxia-inducible factor prolyl hydroxylase activity in cardiomyocytes phenocopies ischemic cardiomyopathy.

Preventing cardiac remodeling: the combination of cell-based therapy and cardiac support therapy preserves left ventricular function in rodent model of myocardial ischemia.

Telomere dysfunction induces metabolic and mitochondrial compromise.

Notch1 in bone marrow-derived cells mediates cardiac repair after myocardial infarction.

Echocardiographic speckle-tracking based strain imaging for rapid cardiovascular phenotyping in mice.

Evidence for human lung stem cells.

Molecular MRI of acute necrosis with a novel DNA-binding gadolinium chelate: kinetics of cell death and clearance in infarcted myocardium.

Nanoparticles targeting the infarcted heart.

Doxycycline reduces fibril formation in a transgenic mouse model of AL amyloidosis.

Wnt signaling exerts an antiproliferative effect on adult cardiac progenitor cells through IGFBP3.

Current perspectives on cardiac amyloidosis.

Homocysteine induces cardiomyocyte dysfunction and apoptosis through p38 MAPK-mediated increase in oxidant stress.

AMPK isoform expression in the normal and failing hearts.

Cardiac side population cells: moving toward the center stage in cardiac regeneration.

The continuing evolution of the Langendorff and ejecting murine heart: new advances in cardiac phenotyping.

Optimized ventricular restraint therapy: adjustable restraint is superior to standard restraint in an ovine model of ischemic cardiomyopathy.

Spot identification and quality control in cell-based microarrays.

Regeneration in heart disease-Is ECM the key?

Abcg2 Regulates Cell Cycle Progression and Asymmetric Division in Mouse Cardiac Side Population Progenitor Cells.

Adult cardiac progenitor cell aggregates exhibit survival benefit both in vitro and in vivo.

PGC1α plays a critical role in TWEAK-induced cardiac dysfunction.

Fluorescence tomography of rapamycin-induced autophagy and cardioprotection in vivo.

Regional cardiac dysfunction and dyssynchrony in a murine model of afterload stress.

mir-17-92 cluster is required for and sufficient to induce cardiomyocyte proliferation in postnatal and adult hearts.

Human amyloidogenic light chain proteins result in cardiac dysfunction, cell death, and early mortality in zebrafish.

Methods to study the proliferation and differentiation of cardiac side population (CSP) cells.

Stanniocalcin1 is a key mediator of amyloidogenic light chain induced cardiotoxicity.

MicroRNA-26a regulates pathological and physiological angiogenesis by targeting BMP/SMAD1 signaling.

Identification of apolipoprotein D as a cardioprotective gene using a mouse model of lethal atherosclerotic coronary artery disease.

Flt3 activation improves post-myocardial infarction remodeling involving a cytoprotective effect on cardiomyocytes.

Gradient static-strain stimulation in a microfluidic chip for 3D cellular alignment.

Microfluidics-assisted fabrication of gelatin-silica core-shell microgels for injectable tissue constructs.

Regenerative therapy for cardiovascular disease.

A systematic survey of lipids across mouse tissues.

Cardiac stem cells: biology and clinical applications.

Microstructural impact of ischemia and bone marrow-derived cell therapy revealed with diffusion tensor magnetic resonance imaging tractography of the heart in vivo.

Ly-6Chigh monocytes depend on Nr4a1 to balance both inflammatory and reparative phases in the infarcted myocardium.

Identifying early changes in myocardial microstructure in hypertensive heart disease.

Worming along in amyloid cardiotoxicity.

Lysosomal dysfunction and impaired autophagy underlie the pathogenesis of amyloidogenic light chain-mediated cardiotoxicity.

A role for matrix stiffness in the regulation of cardiac side population cell function.

Lysosomal dysfunction and impaired autophagy underlie the pathogenesis of amyloidogenic light chain-mediated cardiotoxicity.

MicroRNA-34a Plays a Key Role in Cardiac Repair and Regeneration Following Myocardial Infarction.

Convergences of Life Sciences and Engineering in Understanding and Treating Heart Failure.

Alteration in ventricular pressure stimulates cardiac repair and remodeling.

Quantitative [F]florbetapir PET/CT may identify lung involvement in patients with systemic AL amyloidosis.

Harnessing Cardiac Regeneration as a Potential Therapeutic Strategy for AL Cardiac Amyloidosis.

Natural Compound Library Screening Identifies New Molecules for the Treatment of Cardiac Fibrosis and Diastolic Dysfunction.

Mitochondrial MUL1 E3 ubiquitin ligase regulates Hypoxia Inducible Factor (HIF-1α) and metabolic reprogramming by modulating the UBXN7 cofactor protein.