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Updated: Sep 1, 2025

Investigating Aortic Valve Calcification via Isolation and Culture of T Lymphocytes using Feeder Cells from Irradiated Buffy Coat
Published on: February 4, 2021
PTP1B Inhibition Improves Mitochondrial Dynamics to Alleviate Calcific Aortic Valve Disease Via Regulating
Feng Liu1,2, Jinyong Chen1,2, Wangxing Hu1,2
1Department of Cardiology of The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Abstract:
There are currently no pharmacological therapies for calcific aortic valve disease (CAVD). Here, we evaluated the role of protein tyrosine phosphatase 1B (PTP1B) inhibition in CAVD. Up-regulation of PTP1B was critically involved in calcified human aortic valve, and PTP1B inhibition had beneficial effects in preventing fibrocalcific response in valvular interstitial cells and LDLR-/- mice. In addition, we reported a novel function of PTP1B in regulating mitochondrial homeostasis by interacting with the OPA1 isoform transition in valvular interstitial cell osteogenesis. Thus, these findings have identified PTP1B as a potential target for preventing aortic valve calcification in patients with CAVD.
Insights
Protein tyrosine phosphatase 1B (PTP1B) inhibition shows promise for treating calcific aortic valve disease (CAVD). Targeting PTP1B may prevent aortic valve calcification by preserving mitochondrial function.
Area of Science:
- Biochemistry
- Cardiovascular Biology
- Pharmacology
Background:
- Calcific aortic valve disease (CAVD) lacks effective pharmacological treatments.
- Protein tyrosine phosphatase 1B (PTP1B) is implicated in disease pathogenesis.
Purpose of the Study:
- To investigate the role of PTP1B in CAVD.
- To evaluate the therapeutic potential of PTP1B inhibition in CAVD.
Main Methods:
- Assessed PTP1B expression in human calcified aortic valves.
- Examined the effects of PTP1B inhibition on valvular interstitial cells and LDLR-/- mice.
- Investigated PTP1B's interaction with OPA1 in mitochondrial homeostasis and osteogenesis.
Main Results:
- PTP1B was upregulated in calcified human aortic valves.
- PTP1B inhibition reduced the fibrocalcific response in vitro and in vivo.
- PTP1B regulates mitochondrial homeostasis via OPA1 isoform transition, impacting valvular interstitial cell osteogenesis.
Conclusions:
- PTP1B plays a critical role in CAVD pathogenesis.
- PTP1B inhibition demonstrates therapeutic potential for CAVD.
- Targeting PTP1B may offer a novel strategy for preventing aortic valve calcification.
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