0000000000341633

AUTHOR

Janne T. Backman

0000-0002-9577-2788

showing 2 related works from this author

Prevention of chemotherapy-induced cachexia by ACVR2B ligand blocking has different effects on heart and skeletal muscle

2017

Background Toxicity of chemotherapy on skeletal muscles and the heart may significantly contribute to cancer cachexia, mortality, and decreased quality of life. Doxorubicin (DOX) is an effective cytostatic agent, which unfortunately has toxic effects on many healthy tissues. Blocking of activin receptor type IIB (ACVR2B) ligands is an often used strategy to prevent skeletal muscle loss, but its effects on the heart are relatively unknown. Methods The effects of DOX treatment with or without pre-treatment with soluble ACVR2B-Fc (sACVR2B-Fc) were investigated. The mice were randomly assigned into one of the three groups: (1) vehicle (PBS)-treated controls, (2) DOX-treated mice (DOX), and (3) …

0301 basic medicinemedicine.medical_specialtyTransferrin receptorMyostatinCachexia03 medical and health sciences0302 clinical medicineAtrophyPhysiology (medical)Internal medicinemedicineOrthopedics and Sports MedicineDoxorubicinbiologybusiness.industrySkeletal muscleActivin receptormedicine.disease3. Good health030104 developmental biologymedicine.anatomical_structureEndocrinology030220 oncology & carcinogenesisbiology.proteinbusinessACVR2Bmedicine.drugJournal of Cachexia, Sarcopenia and Muscle
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VEGF-B gene therapy inhibits doxorubicin-induced cardiotoxicity by endothelial protection

2016

Congestive heart failure is one of the leading causes of disability in long-term survivors of cancer. The anthracycline antibiotic doxorubicin (DOX) is used to treat a variety of cancers, but its utility is limited by its cumulative cardiotoxicity. As advances in cancer treatment have decreased cancer mortality, DOX-induced cardiomyopathy has become an increasing problem. However, the current means to alleviate the cardiotoxicity of DOX are limited. We considered that vascular endothelial growth factor-B (VEGF-B), which promotes coronary arteriogenesis, physiological cardiac hypertrophy, and ischemia resistance, could be an interesting candidate for prevention of DOX-induced cardiotoxicity …

0301 basic medicineMaleVEGFBVascular Endothelial Growth Factor BAnthracyclineAdipose Tissue WhiteCardiomyopathyheart failureApoptosisheart030204 cardiovascular system & hematologyPharmacologyta3111Mitochondria Heart03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorNeoplasmsmedicinepolycyclic compoundscancerAnimalsDoxorubicinTube formationCardiotoxicityMultidisciplinaryAntibiotics Antineoplasticbusiness.industryta1184MyocardiumEndothelial CellsGenetic TherapyBiological Sciencesmedicine.diseaseCardiotoxicity3. Good healthVascular endothelial growth factorMice Inbred C57BL030104 developmental biologychemistryLiverDoxorubicinHeart failureendothelial cellArteriogenesisbusinessmedicine.drugDNA Damage
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