Article in Circulation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing 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.
Maartje Westhoff *Department of Physiology and Membrane Biology (M.W., T.L.V., S.G.D.V., E.J.D., R.E.D.), University of California, Davis.ORCID 0000-0002-5421-8609
Taylor L Voelker *Department of Physiology and Membrane Biology (M.W., T.L.V., S.G.D.V., E.J.D., R.E.D.), University of California, Davis.ORCID 0000-0002-6779-9350
Silvia G Del VillarDepartment of Physiology and Membrane Biology (M.W., T.L.V., S.G.D.V., E.J.D., R.E.D.), University of California, Davis.
Phung N ThaiDivision of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis (P.N.T., F.F.R., P.S., N.C.).ORCID 0000-0001-7344-150X
Hannah M VoorheesDepartment of Pharmacology (H.M.V., J.L.M., J.B., N.C., M.N.-C.), University of California, Davis.ORCID 0009-0007-1289-8267
Fatin Fazrina RoslanDivision of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis (P.N.T., F.F.R., P.S., N.C.).
Jody L MartinDepartment of Pharmacology (H.M.V., J.L.M., J.B., N.C., M.N.-C.), University of California, Davis.ORCID 0000-0001-5607-3338
Julie BossuytDepartment of Pharmacology (H.M.V., J.L.M., J.B., N.C., M.N.-C.), University of California, Davis.ORCID 0000-0001-8874-4765
Padmini SirishDivision of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis (P.N.T., F.F.R., P.S., N.C.).
Nipavan ChiamvimonvatDepartment of Pharmacology (H.M.V., J.L.M., J.B., N.C., M.N.-C.), University of California, Davis.ORCID 0000-0001-9499-8817
Madeline Nieves-CintrónDepartment of Pharmacology (H.M.V., J.L.M., J.B., N.C., M.N.-C.), University of California, Davis.ORCID 0000-0003-1935-8400
Eamonn J DicksonDepartment of Physiology and Membrane Biology (M.W., T.L.V., S.G.D.V., E.J.D., R.E.D.), University of California, Davis.ORCID 0000-0001-8619-7630
Rose E DixonDepartment of Physiology and Membrane Biology (M.W., T.L.V., S.G.D.V., E.J.D., R.E.D.), University of California, Davis.ORCID 0000-0003-0655-690X
Funding
Molecular choreography of CaV1.2 channels in the aging myocardiumR01AG063796 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Rose Ellen Dixon · 2019 to 2026
$3.1M
Lipid regulation of Cardiac Excitation-Contraction couplingR01HL159304 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI DIXON, ROSE ELLEN · 2022 to 2025
$2.4M
Mechanisms of VSM dysfunction in diabetes and HFpEFR01HL171014 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Manuel F Navedo, Madeline Nieves-Cintron · 2024 to 2026
$2.0M
Alpha-Synuclein aberrantly modifies the nanoscale distribution and function of ion channels to promote neuronal cytotoxicityRF1NS131379 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI DICKSON, EAMONN JAMES · 2023 to 2023
$1.7M
Lysosomal control of plasma membrane -endoplasmic reticulum membrane contacts regulates neuronal excitabilityR35GM149211 · NIGMS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Eamonn James Dickson · 2023 to 2026
backgroundContractile dysfunction, hypertrophy, and cell death during heart failure are linked to altered Ca
methodsMice received 1-week infusions of AngII, bisperoxovanadium (1,10 phenanthroline), both, or saline via osmotic minipumps. We used mass spectrometry, super-resolution microscopy, electrophysiology, confocal imaging, immunoblot, echocardiography, and histology to assess phosphoinositide levels, L-type voltage-gated calcium channel Ca
resultsChronic AngII infusion caused widespread phosphoinositide imbalance, reducing phosphatidylinositol, phosphatidylinositol phosphate, phosphatidylinositol bisphosphate, and phosphatidylinositol (3,4,5)-trisphosphate levels. Ca
conclusionsThese findings reveal a complex interplay between phosphoinositide signaling, ion channel trafficking, and compensatory phospho-regulation in AngII-induced cardiac pathology. We establish phosphatidylinositol (3,4,5)-trisphosphate depletion as a critical link between chronic AngII signaling and cardiac dysfunction. The dissociation between persistent cellular remodeling and preserved organ function with PTEN inhibition reveals that cardioprotection occurs primarily through reduced fibrosis. PTEN inhibition, thus, emerges as a promising therapeutic strategy for heart failure associated with pathological renin-angiotensin system activation, with potential to complement existing therapies by targeting antifibrotic responses.
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 OpenQuestion graph.
Phosphoinositide Depletion and Compensatory Phospho-Signaling in Angiotensin II-Induced Heart Disease. · full record | OpenQuestion