Verina H. Leung
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Verina H. Leung has a total of 19 co-authors. Here are the top co-authors by number of shared publications:
- Antonina I. Frolova
Washington University School of Medicine
1 shared publication - Ardem Patapoutian
Howard Hughes Medical Institute, Department of Neuroscience, Dorris Neuroscience Center, Scripps Research, La Jolla, USA
1 shared publication - Darren J. Lipomi
Aiiso Yufeng Li Family Department of Chemical and Nano Engineering, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093-0448, United States
1 shared publication - Li Ye
Department of Neuroscience, Dorris Neuroscience Center, Scripps Research, San Diego, CA, USA; Howard Hughes Medical Institute, Chevy Chase, MD, USA
1 shared publication - Manuel Sanchez-Alavez
Department of Molecular and Cellular Biology The Scripps Research Institute La Jolla California USA
1 shared publication - Martha Rocio Servín-Vences
Department of Neuroscience, Dorris Neuroscience Center, The Scripps Research Institute, San Diego, CA, USA
1 shared publication
Latest Publications
- Top Cited PapersOpen Access
- 13 November 2025
- Published by American Association for the Advancement of Science (AAAS) in Science
- Vol. 390 (6774) , eady3045
PIEZO channels link mechanical forces to uterine contractions in parturition
Mechanical forces are extensively involved in pregnancy and parturition, but their precise roles and mechanisms remain poorly understood. We identified mechanically activated ion channels PIEZO1 and PIEZO2 as key mechanotransducers required for labor progression. Genetic deletion of Piezo1 and Piezo2 in mice resulted in weakened uterine contractions and severe parturition defects. Tissue-specific knockouts revealed that deletion in either uterus or sensory neurons alone caused modest defects whereas combined loss markedly impaired labor, demonstrating additive effects. Single-nuclei sequencing indicated that loss of PIEZO function reduced expression of connexin43 ( Gja1 ), a gap junction protein in uterine smooth muscle cells, suggesting a mechanistic link to impaired contraction. These findings highlight the critical role of PIEZO channels in mechanotransduction during parturition and suggest therapeutic targets for labor dysfunction.
- 13 November 2025
- Published by American Association for the Advancement of Science (AAAS) in Science
- Vol. 390 (6774) , eady3045
Top Cited PapersOpen AccessPIEZO channels link mechanical forces to uterine contractions in parturition
Mechanical forces are extensively involved in pregnancy and parturition, but their precise roles and mechanisms remain poorly understood. We identified mechanically activated ion channels PIEZO1 and PIEZO2 as key mechanotransducers required for labor progression. Genetic deletion of Piezo1 and Piezo2 in mice resulted in weakened uterine contractions and severe parturition defects. Tissue-specific knockouts revealed that deletion in either uterus or sensory neurons alone caused modest defects whereas combined loss markedly impaired labor, demonstrating additive effects. Single-nuclei sequencing indicated that loss of PIEZO function reduced expression of connexin43 ( Gja1 ), a gap junction protein in uterine smooth muscle cells, suggesting a mechanistic link to impaired contraction. These findings highlight the critical role of PIEZO channels in mechanotransduction during parturition and suggest therapeutic targets for labor dysfunction.