Article in Science translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
18 authors.
Amit ManhasStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.ORCID 0000-0001-6044-4576
Yu LiuStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.ORCID 0000-0001-7110-127X
Chikage NoishikiStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.ORCID 0000-0002-4623-1176
David WuStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.ORCID 0000-0002-1193-8307
Dipti TripathiStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
Sarah MirzaStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.ORCID 0009-0002-6350-3054
Dilip ThomasStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.ORCID 0000-0001-7427-5523
Lu LiuStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.ORCID 0000-0002-5762-1751
Avirup GuhaDepartment of Medicine, Division of Cardiology, and Vascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA.ORCID 0000-0003-0253-1174
Patricia K NguyenStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.ORCID 0000-0001-7170-9787
Ian Y ChenStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
Vipul ChitaliaRenal Section, Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA.ORCID 0000-0002-6663-6058
Paul ChengStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.ORCID 0000-0003-3429-2702
Danish SayedDepartment of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, NJ 07103, USA.
Melinda L TelliDivision of Oncology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.ORCID 0000-0001-7993-1235
Karim SallamStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
Joseph C WuStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.ORCID 0000-0002-6068-8041
Nazish SayedStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.ORCID 0000-0002-8229-721X
Funding
Modeling Tyrosine Kinase Inhibitor-Induced Vascular Dysfunction Using Human iPSCsR01HL141851 · NHLBI · STANFORD UNIVERSITY · PI WONG, WING H., WU, JOSEPH C. · 2018 to 2025
$5.7M
Single Cell Sequencing of Human iPSC-CM Subtype Identity and FunctionR01HL145676 · NHLBI · STANFORD UNIVERSITY · PI MARK MERCOLA, Joseph C. Wu · 2019 to 2026
$5.1M
Elucidating Anthracycline-Induced Cell Type-Specific Cardiovascular Toxicity with CRISPRi/a ScreensR01HL150693 · NHLBI · STANFORD UNIVERSITY · PI Ronglih Liao, Joseph C. Wu · 2021 to 2026
$4.1M
Deciphering the Endothelial Cell-Cardiomyocyte Crosstalk in LMNA CardiomyopathyR01HL158641 · NHLBI · STANFORD UNIVERSITY · PI SAYED, NAZISH · 2021 to 2025
$2.2M
Unraveling the role of endothelium in chemotherapy-induced cardiotoxicityR01HL161002 · NHLBI · STANFORD UNIVERSITY · PI SAYED, NAZISH · 2022 to 2025
$1.6M
Unraveling Proteasome Inhibitor-Induced Cardiovascular Toxicity through Integrative MultiomicsR01HL176822 · NHLBI · STANFORD UNIVERSITY · PI MARK MERCOLA, Joseph C. Wu · 2025 to 2026
$1.4M
Modeling Endothelial Dysfunction in LMNA-related Dilated CardiomyopathyK01HL135455 · NHLBI · STANFORD UNIVERSITY · PI SAYED, NAZISH · 2017 to 2021
Tyrosine kinase inhibitors (TKIs) have improved cancer outcomes but are limited by cardiovascular toxicity, most notably hypertension and heart failure. The underlying mechanisms remain poorly understood, hindering the development of protective strategies. Here, we investigated the role of endothelial mechanotransduction in mediating vascular and cardiac injury caused by the vascular endothelial growth factor receptor-targeting TKI sunitinib. Using patient-specific induced pluripotent stem cell-derived endothelial cells (iPSC-ECs) and a mouse model of TKI-induced hypertension, we identified down-regulation of
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.
Multiscale profiling of tyrosine kinase inhibitor cardiotoxicity reveals mechanosensitive ion channel PIEZO1 as cardioprotective. · full record | Socratic