Erratum to: Low‐intensity pulsed ultrasound ameliorates angiotensin II-induced cardiac fibrosis by alleviating inflammation via a caveolin-1-dependent pathway
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Erratum|Updated:2024-09-20
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Erratum to: Low‐intensity pulsed ultrasound ameliorates angiotensin II-induced cardiac fibrosis by alleviating inflammation via a caveolin-1-dependent pathway
Erratum to: Low‐intensity pulsed ultrasound ameliorates angiotensin II-induced cardiac fibrosis by alleviating inflammation via a caveolin-1-dependent pathway
Erratum to: Low‐intensity pulsed ultrasound ameliorates angiotensin II-induced cardiac fibrosis by alleviating inflammation via a caveolin-1-dependent pathway
Journal of Zhejiang University-SCIENCE B (Biomedicine & Biotechnology)Journal of Zhejiang University-SCIENCE B (Biomedicine & Biotechnology)Vol. 25, Issue 9, Pages: 800(2024)
Affiliations:
1.Department of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China
2.Key Laboratory of Modern Acoustics, Department of Physics, Collaborative Innovation Center of Advanced Microstructure, Nanjing University, Nanjing 210093, China
3.Departments of Genetics, Pediatrics, and Medicine (Cardiology), Wilf Cardiovascular Research Institute, Albert Einstein College of Medicine, Bronx, NY 10461, USA;Erratum to: J Zhejiang Univ-Sci B (Biomed & Biotechnol) 2021 22
Kun ZHAO, Jing ZHANG, Tianhua XU, et al. Erratum to: Low‐intensity pulsed ultrasound ameliorates angiotensin II-induced cardiac fibrosis by alleviating inflammation via a caveolin-1-dependent pathway. [J]. Journal of Zhejiang University-SCIENCE B (Biomedicine & Biotechnology) 25(9):800(2024)
DOI:
Kun ZHAO, Jing ZHANG, Tianhua XU, et al. Erratum to: Low‐intensity pulsed ultrasound ameliorates angiotensin II-induced cardiac fibrosis by alleviating inflammation via a caveolin-1-dependent pathway. [J]. Journal of Zhejiang University-SCIENCE B (Biomedicine & Biotechnology) 25(9):800(2024) DOI: 10.1631/jzus.B21e0130.
Erratum to: Low‐intensity pulsed ultrasound ameliorates angiotensin II-induced cardiac fibrosis by alleviating inflammation via a caveolin-1-dependent pathway