血管紧张素Ⅱ诱导的心脏病中的磷酸肌醇耗竭和代偿性磷酸信号传导：通过PTEN抑制进行保护。
Westhoff, M., Voelker, T.L., Villar, S.G.D., Thai, P.N., Voorhees, H.M., Roslan, F.F., Martin, J.L., Bossuyt, J., Sirish, P., Chiamvimonvat, N., Nieves-Cintrón, M., Dickson, E.J., & Dixon, R.E. (2026). Phosphoinositide Depletion and Compensatory Phospho-Signaling in Angiotensin II-Induced Heart Disease: Protection Through PTEN Inhibition.. Circ Res. https://doi.org/10.1161/CIRCRESAHA.125.327896
Westhoff M, Voelker TL, Villar SGD, Thai PN, Voorhees HM, Roslan FF, et al. Phosphoinositide Depletion and Compensatory Phospho-Signaling in Angiotensin II-Induced Heart Disease: Protection Through PTEN Inhibition.. Circ Res. 2026; doi: 10.1161/CIRCRESAHA.125.327896
Westhoff M, Voelker TL, Villar SGD, et al. Phosphoinositide Depletion and Compensatory Phospho-Signaling in Angiotensin II-Induced Heart Disease: Protection Through PTEN Inhibition.[J]. Circ Res. 2026. DOI: 10.1161/CIRCRESAHA.125.327896.
@article{westhoff2026,
author = {Maartje Westhoff and Taylor L Voelker and Silvia G Del Villar and Phung N Thai and Hannah M Voorhees and Fatin Fazrina Roslan and Jody L Martin and Julie Bossuyt and Padmini Sirish and Nipavan Chiamvimonvat and Madeline Nieves-Cintrón and Eamonn J Dickson and Rose E Dixon},
title = {Phosphoinositide Depletion and Compensatory Phospho-Signaling in Angiotensin II-Induced Heart Disease: Protection Through PTEN Inhibition.},
journal = {Circ Res},
year = {2026},
doi = {10.1161/CIRCRESAHA.125.327896},
note = {PMID: 41859814},
}
TY - JOUR AU - Maartje Westhoff AU - Taylor L Voelker AU - Silvia G Del Villar AU - Phung N Thai AU - Hannah M Voorhees AU - Fatin Fazrina Roslan AU - Jody L Martin AU - Julie Bossuyt AU - Padmini Sirish AU - Nipavan Chiamvimonvat AU - Madeline Nieves-Cintrón AU - Eamonn J Dickson AU - Rose E Dixon TI - Phosphoinositide Depletion and Compensatory Phospho-Signaling in Angiotensin II-Induced Heart Disease: Protection Through PTEN Inhibition. T2 - Circ Res PY - 2026 DO - 10.1161/CIRCRESAHA.125.327896 AN - PMID:41859814 ER -
Contractile dysfunction, hypertrophy, and cell death during heart failure are linked to altered Ca Mice 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 PI levels, Ca Chronic AngII infusion caused widespread PI imbalance, reducing PI, phosphatidylinositol (4,5)-bisphosphate, and phosphatidylinositol (3,4,5)-trisphosphate levels. Ca These findings reveal a complex interplay between PI 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.