0000000000544671

AUTHOR

Ruizhu Lin

0000-0003-0796-0955

showing 3 related works from this author

Systemic blockade of ACVR2B ligands attenuates muscle wasting in ischemic heart failure without compromising cardiac function

2020

Signaling through activin receptors regulates skeletal muscle mass and activin receptor 2B (ACVR2B) ligands are also suggested to participate in myocardial infarction (MI) pathology in the heart. In this study, we determined the effect of systemic blockade of ACVR2B ligands on cardiac function in experimental MI, and defined its efficacy to revert muscle wasting in ischemic heart failure (HF). Mice were treated with soluble ACVR2B decoy receptor (ACVR2B-Fc) to study its effect on post-MI cardiac remodeling and on later HF. Cardiac function was determined with echocardiography, and myocardium analyzed with histological and biochemical methods for hypertrophy and fibrosis. Pharmacological blo…

soluviestintägrowth differentiation factorsmyocardial infarctionactivinssydäninfarktisydänlihassolut
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Systemic blockade of ACVR2B ligands attenuates muscle wasting in ischemic heart failure without compromising cardiac function

2020

Signaling through activin receptors regulates skeletal muscle mass and activin receptor 2B (ACVR2B) ligands are also suggested to participate in myocardial infarction (MI) pathology in the heart. In this study, we determined the effect of systemic blockade of ACVR2B ligands on cardiac function in experimental MI, and defined its efficacy to revert muscle wasting in ischemic heart failure (HF). Mice were treated with soluble ACVR2B decoy receptor (ACVR2B-Fc) to study its effect on post-MI cardiac remodeling and on later HF. Cardiac function was determined with echocardiography, and myocardium analyzed with histological and biochemical methods for hypertrophy and fibrosis. Pharmacological blo…

Male0301 basic medicineCardiac function curvemedicine.medical_specialtyActivin Receptors Type IIMyocardial IschemiaMyostatinBiochemistryMuscle hypertrophyMice03 medical and health sciences0302 clinical medicineInternal medicineGeneticsmedicineAnimalsMyocyteMyocardial infarctionMolecular BiologyVentricular Remodelingbiologybusiness.industrySkeletal muscleHeartmedicine.disease3. Good healthBlockadeMice Inbred C57BLDisease Models AnimalMuscular Atrophy030104 developmental biologymedicine.anatomical_structureCardiologybiology.proteinbusiness030217 neurology & neurosurgeryACVR2BSignal TransductionTranscription FactorsBiotechnologyThe FASEB Journal
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Systemic blockade of ACVR2B ligands protects myocardium from acute ischemia-reperfusion injury

2019

Activin A and myostatin, members of the transforming growth factor (TGF)-β superfamily of secreted factors, are potent negative regulators of muscle growth, but their contribution to myocardial ischemia-reperfusion (IR) injury is not known. The aim of this study was to investigate if activin 2B (ACVR2B) receptor ligands contribute to myocardial IR injury. Mice were treated with soluble ACVR2B decoy receptor (ACVR2B-Fc) and subjected to myocardial ischemia followed by reperfusion for 6 or 24 h. Systemic blockade of ACVR2B ligands by ACVR2B-Fc was protective against cardiac IR injury, as evidenced by reduced infarcted area, apoptosis, and autophagy and better preserved LV systolic function fo…

MaleActivin Receptors Type IIiskemialihaksetSmad2 ProteinMyostatinPharmacologyMice0302 clinical medicineDrug DiscoverykasvutekijätMyocytes CardiacCardioprotection0303 health sciences318 Medical biotechnologybiologysydänactivins1184 Genetics developmental biology physiologyII RECEPTORS3. Good health030220 oncology & carcinogenesisMolecular MedicineOriginal ArticleSignal TransductionCardiac function curvegrowth differentiation factorsProgrammed cell deathBLOCKINGischemia-reperfusion injuryIschemiaMyocardial Reperfusion InjuryMASSta311103 medical and health sciencesMYOSTATIN-KNOCKOUTCARDIOPROTECTIONGeneticsmedicineAnimalsMolecular Biologylihassolut030304 developmental biologyPharmacologySKELETAL-MUSCLE GROWTHbusiness.industryMyocardiumFOLLISTATINMyostatinmedicine.diseaseACVR2BMice Inbred C57BLACTIVIN-AGDF11GDF11biology.protein3111 BiomedicineproteiinitbusinessReperfusion injuryDIFFERENTIATION FACTOR 11ACVR2BTranscription Factors
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