0000000001137144

AUTHOR

Tanja Holopainen

showing 2 related works from this author

Endothelial Bmx tyrosine kinase activity is essential for myocardial hypertrophy and remodeling

2015

Cardiac hypertrophy accompanies many forms of heart disease, including ischemic disease, hypertension, heart failure, and valvular disease, and it is a strong predictor of increased cardiovascular morbidity and mortality. Deletion of bone marrow kinase in chromosome X (Bmx), an arterial nonreceptor tyrosine kinase, has been shown to inhibit cardiac hypertrophy in mice. This finding raised the possibility of therapeutic use of Bmx tyrosine kinase inhibitors, which we have addressed here by analyzing cardiac hypertrophy in gene-targeted mice deficient in Bmx tyrosine kinase activity. We found that angiotensin II (Ang II)-induced cardiac hypertrophy is significantly reduced in mice deficient i…

medicine.medical_specialtyendotheliumEndotheliumAngiogenesiscardiomyocyteCardiomegalyheartmTORC1030204 cardiovascular system & hematologyMitochondria Heart03 medical and health sciencesMice0302 clinical medicineInternal medicinemedicineAnimalsMyocytes Cardiac030304 developmental biologyMice Knockout0303 health sciencesMultidisciplinaryKinasebusiness.industryta1184Angiotensin IIBiological SciencesProtein-Tyrosine KinasesAngiotensin IImedicine.anatomical_structureEndocrinologyEtkcardiovascular systemCancer researchPhosphorylationCytokinesEndothelium VascularSignal transductionInflammation MediatorssignalingbusinessTyrosine kinaseSignal Transduction
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Treating cachexia using soluble ACVR2B improves survival, alters mTOR localization, and attenuates liver and spleen responses.

2018

Background Cancer cachexia increases morbidity and mortality, and blocking of activin receptor ligands has improved survival in experimental cancer. However, the underlying mechanisms have not yet been fully uncovered. Methods The effects of blocking activin receptor type 2 (ACVR2) ligands on both muscle and non‐muscle tissues were investigated in a preclinical model of cancer cachexia using a recombinant soluble ACVR2B (sACVR2B‐Fc). Treatment with sACVR2B‐Fc was applied either only before the tumour formation or with continued treatment both before and after tumour formation. The potential roles of muscle and non‐muscle tissues in cancer cachexia were investigated in order to understand th…

MaleTUMOR-BEARING MICElcsh:Diseases of the musculoskeletal systemCachexiaprotein synthesisActivin Receptors Type IIMDSCphysical activityAcute phase responseKaplan-Meier EstimateACTIVATIONActivinMiceNeoplasmsOrthopedics and Sports MedicineTOR Serine-Threonine Kinasesactivinlcsh:Human anatomyII RECEPTORSRecombinant ProteinsProtein TransportLivermyostatinPROTEIN-SYNTHESISSKELETAL-MUSCLECytokinessyöpätauditInflammation MediatorsACUTE-PHASE RESPONSE3122 CancersINHIBITIONlcsh:QM1-695acute phase responsePhysiology (medical)Cell Line TumorAnimalsHumansMuscle SkeletalActivin; Acute phase response; MDSC; Myostatin; Physical activity; Protein synthesis; Orthopedics and Sports Medicine; Physiology (medical)Physical activityMyeloid-Derived Suppressor CellsMyostatinXenograft Model Antitumor AssaysDisease Models AnimalACTIVIN-APHYSICAL-ACTIVITY3121 General medicine internal medicine and other clinical medicineproteiinitEXPERIMENTAL CANCER CACHEXIAlcsh:RC925-935Protein synthesislihassurkastumasairaudetBiomarkersSpleenJournal of cachexia, sarcopenia and muscle
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