Coronary microvascular pericytes are the cellular target of sunitinib malate-induced cardiotoxicity.
about
Human myocardial pericytes: multipotent mesodermal precursors exhibiting cardiac specificity.PET Metabolic Biomarkers for CancerCancer therapy-induced cardiotoxicity: basic mechanisms and potential cardioprotective therapies.Traumatic brain injury results in rapid pericyte loss followed by reactive pericytosis in the cerebral cortex.Targeting of the breast cancer microenvironment with a potent and linkable oxindole based antiangiogenic small molecule.Retrospective analysis of the safety and efficacy of high-dose interleukin-2 after prior tyrosine kinase inhibitor therapy in patients with advanced renal cell carcinoma.Machine learning-based prediction of drug-drug interactions by integrating drug phenotypic, therapeutic, chemical, and genomic propertiesMyocardin-related transcription factors control the motility of epicardium-derived cells and the maturation of coronary vessels.Physiological, pharmacological and toxicological considerations of drug-induced structural cardiac injuryA PKM2 signature in the failing heart.Nonsteroidal anti-inflammatory drugs alter vasa recta diameter via pericytes.A Novel Positron Emission Tomography (PET) Approach to Monitor Cardiac Metabolic Pathway Remodeling in Response to Sunitinib Malate.LPS causes pericyte loss and microvascular dysfunction via disruption of Sirt3/angiopoietins/Tie-2 and HIF-2α/Notch3 pathways.Vascular Toxicities of Cancer Therapies: The Old and the New--An Evolving Avenue.Cardio-Oncology: How New Targeted Cancer Therapies and Precision Medicine Can Inform Cardiovascular Discovery.Discovery of pan-VEGF inhibitory peptides directed to the extracellular ligand-binding domains of the VEGF receptors.Animal models in studies of cardiotoxicity side effects from antiblastic drugs in patients and occupational exposed workersThe role of pericytes in neurovascular unit remodeling in brain disorders.Recognizing and managing left ventricular dysfunction associated with therapeutic inhibition of the vascular endothelial growth factor signaling pathway.Conquests and perspectives of cardio-oncology in the field of tumor angiogenesis-targeting tyrosine kinase inhibitor-based therapy.Tyrosine kinase-targeting drugs-associated heart failure.Targeting vascular and leukocyte communication in angiogenesis, inflammation and fibrosis.SCAI Expert consensus statement: Evaluation, management, and special considerations of cardio-oncology patients in the cardiac catheterization laboratory (endorsed by the cardiological society of india, and sociedad Latino Americana de Cardiologıa iCardiac Complications of Cancer Therapy: Pathophysiology, Identification, Prevention, Treatment, and Future Directions.Extract of Calvatia gigantea inhibits proliferation of A549 human lung cancer cells.Tyrosine Kinase Inhibitors and Vascular Toxicity: Impetus for a Classification System?Beyond Anthracyclines: Preemptive Management of Cardiovascular Toxicity in the Era of Targeted Agents for Hematologic Malignancies.Skeletal and cardiac muscle pericytes: Functions and therapeutic potential.Generation, expansion and functional analysis of endothelial cells and pericytes derived from human pluripotent stem cells.Lessons learned from adult clinical experience to inform evaluations of VEGF pathway inhibitors in children with cancer.Cardiotoxic drugs Herceptin and doxorubicin inhibit cardiac microvascular endothelial cell barrier formation resulting in increased drug permeability.Toxicity and response in cats with neoplasia treated with toceranib phosphate.Cardiac Metabolic Deregulation Induced by the Tyrosine Kinase Receptor Inhibitor Sunitinib is rescued by Endothelin Receptor AntagonismCardiotoxicity of cancer chemotherapy: identification, prevention and treatment.Effects of local irradiation combined with sunitinib on early remodeling, mitochondria, and oxidative stress in the rat heartCardio-oncology: it takes two to translate.Pazopanib for renal cell carcinoma leads to elevated mean arterial pressures in a murine model.Comprehensive review of cardiovascular toxicity of drugs and related agents.Cardiovascular Toxicities of Small Molecule Tyrosine Kinase Inhibitors: An Opportunity for Systems-Based Approaches.Antineoplastic Drug-Induced Cardiotoxicity: A Redox Perspective.
P2860
Q27329894-7061D9F1-9191-4F08-A25D-2F128D02A17EQ28074449-BC36ECA8-4CAB-4071-B94A-186F012D9F54Q30426853-7D5E2F0D-EEA0-40C9-B1C2-BC1057D884E0Q30663521-8D8ED4E5-2CE0-4A9E-BEB0-8D8829FD66F0Q33913901-4F72681D-B901-4D82-84DC-3A9059EF8C76Q34021843-11313951-C06B-4CF5-A280-DADDCF781046Q34235803-F129FD11-7A28-4F92-BAB4-D8744A690B74Q34985191-F8D750F5-3EF1-47C3-BCA9-22909187BCE0Q35039202-5EF1940C-1478-4CA4-B8AB-1317C2D3BC4BQ35235782-D58264A6-0629-4743-A78F-80C136F0C595Q36122786-1AC199EB-D76C-4D49-92CB-C831B9FE3974Q36262416-49776AEA-D218-437C-B8F7-6CF047215DDBQ36574347-B7D55995-4F99-4A2E-ABD4-A9D744E7964BQ36755620-633C6121-35AF-40A9-91A5-6C3290C8536DQ36891574-65DE3899-459A-4154-927F-091FE0B3080EQ37388064-1E33343C-5292-41B5-9820-2C49BFF2944BQ37631325-5F5AB2B5-953F-470A-B3C2-254187D98063Q38205364-51520BE1-5E12-4168-9BE1-0ADA7AEA9B71Q38237495-440EDFC4-516F-4997-8E83-63432F07D264Q38286128-51BD54B6-90DF-4758-ABB5-6C59853C3984Q38401605-56503DD1-1C11-442D-B8C6-B84B2529D399Q38650120-7F6E8A03-4B4F-4C5A-8C31-36726F096B7EQ38693165-1ACD1FC6-2A76-4CD0-852E-A0241E78B47FQ38735433-8CE32357-0E89-496B-A2F7-F55A7CD2A7D7Q38798709-AE72545D-80EB-4704-AADA-468B54D80824Q38813467-893F5D69-DEAC-4854-A7A8-6E331CC84474Q38944823-492DC6C2-DDE1-4724-8AC0-6EFC80C56B4CQ38946672-8B3E04C0-9B74-41AA-936C-E9210E0A2981Q39184690-EEFB3DC3-919B-44C9-ADF2-AF0F1A327035Q39204706-37C6D0AA-8FEA-4036-B92D-81530F0E522CQ39472056-8C1F871A-0E80-44E9-A613-EC402BDB30C1Q40793870-5F636076-1B27-4BF1-8DFC-E75DE1AA87A0Q41455445-CB397B78-4B25-4DDF-A855-FC898763093AQ41704131-5BA09F7B-2E28-4E1A-96E1-8FC6E0D2D422Q41902920-223E814F-0145-4683-9B2C-1A05E85D8969Q44228500-759B4CD2-7E21-469B-9E74-F273487C8D42Q47367575-7239D56B-6592-4B30-8D66-2784543E67D5Q47556269-292A1EB4-06FD-4CC3-B40A-77A3DB8A700FQ51348764-E08E3F46-3FB6-4884-96FC-00151E900168Q51760757-1E03A530-A706-49B1-944B-7CFEDE751DAD
P2860
Coronary microvascular pericytes are the cellular target of sunitinib malate-induced cardiotoxicity.
description
2013 nî lūn-bûn
@nan
2013年の論文
@ja
2013年論文
@yue
2013年論文
@zh-hant
2013年論文
@zh-hk
2013年論文
@zh-mo
2013年論文
@zh-tw
2013年论文
@wuu
2013年论文
@zh
2013年论文
@zh-cn
name
Coronary microvascular pericyt ...... malate-induced cardiotoxicity.
@en
type
label
Coronary microvascular pericyt ...... malate-induced cardiotoxicity.
@en
prefLabel
Coronary microvascular pericyt ...... malate-induced cardiotoxicity.
@en
P2093
P2860
P1476
Coronary microvascular pericyt ...... malate-induced cardiotoxicity.
@en
P2093
Aarif Y Khakoo
Aditya Goel
Heinrich Taegtmeyer
James C Culver
Jianhu Zhang
Kenneth Dunner
Mark L Entman
Mary E Dickinson
Meredith L Rees
P2860
P304
P356
10.1126/SCITRANSLMED.3005066
P407
P577
2013-05-01T00:00:00Z