PCSK9 promotes atherosclerosis progression through the FOXO3a autophagy signaling pathway
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By
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Yuanjia Shi
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Jing Zhang
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Lina Dai
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Jie Chen
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Shijia Geng
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Yan Niu
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Chongyang Dong
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Chenlei Li
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Rujin Liu
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Ningxia Zhao
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Xiaomeng Wang
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Zhanfeng Gao
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Xi Yang
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Shang Gao
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June 15, 2026
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Clinical Scorecard: The Role of PCSK9 in Advancing Atherosclerosis via the FOXO3a Autophagy Pathway
At a Glance
| Category | Detail |
|---|
| Condition | |
| Key Mechanisms | PCSK9 modulates autophagy via the FOXO3a pathway, influencing macrophage function and plaque progression. |
| Target Population | |
| Care Setting | |
Key Highlights
- PCSK9 enhances autophagy-related protein expression, promoting atherosclerosis.
- COS reduces PCSK9 expression and mitigates atherosclerotic plaque progression.
- FOXO3a is a critical regulator of autophagy in macrophages.
- Excessive autophagy activation may lead to programmed cell death, impacting atherosclerosis.
Guideline-Based Recommendations
Diagnosis
- Monitor PCSK9 levels and autophagy-related proteins in patients with atherosclerosis.
Management
- Consider PCSK9 inhibitors for patients with high LDL cholesterol and atherosclerosis.
Monitoring & Follow-up
- Assess autophagy flux and related protein levels to evaluate treatment efficacy.
Risks
- Excessive autophagy may lead to programmed cell death, complicating atherosclerosis.
Patient & Prescribing Data
Patients with elevated LDL cholesterol and atherosclerosis risk factors.
COS and PCSK9 inhibitors may reduce atherosclerosis progression by modulating autophagy.
Clinical Best Practices
- Evaluate the role of PCSK9 in individual patient cases of atherosclerosis.
- Incorporate autophagy assessment in the management of atherosclerosis.
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