0000000000192147

AUTHOR

Andrey Anisimov

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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VEGF-B-induced vascular growth leads to metabolic reprogramming and ischemia resistance in the heart

2014

Abstract Angiogenic growth factors have recently been linked to tissue metabolism. We have used genetic gain‐ and loss‐of function models to elucidate the effects and mechanisms of action of vascular endothelial growth factor‐B (VEGF‐B) in the heart. A cardiomyocyte‐specific VEGF‐B transgene induced an expanded coronary arterial tree and reprogramming of cardiomyocyte metabolism. This was associated with protection against myocardial infarction and preservation of mitochondrial complex I function upon ischemia‐reperfusion. VEGF‐B increased VEGF signals via VEGF receptor‐2 to activate Erk1/2, which resulted in vascular growth. Akt and mTORC1 pathways were upregulated and AMPK downregulated, …

VEGF‐Bmedicine.medical_specialtyMedicine (General)AngiogenesiseducationMOUSE HEARTIschemiaVEGF-B610 Medicine & healthmTORC1ischemiaBiologyQH426-470CONTRIBUTESchemistry.chemical_compoundangiogenesisR5-920CARDIAC-FUNCTIONInternal medicinemedicineGeneticsFAILUREta318Myocardial infarctionFATTY-ACID UPTAKEREPERFUSION INJURY610 Medicine & healthProtein kinase BMYOCARDIAL HYPERTROPHYAMPKta3121medicine.diseaseCell biologyARTERIOGENESISVascular endothelial growth factorMICEEndocrinologychemistry3121 General medicine internal medicine and other clinical medicineendothelial cellMolecular Medicine3111 BiomedicineReperfusion injurymetabolism
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