数据日期 2026-10-29 · 生成时间 2026-10-29 06:03
证据级别：摘要级。本条依据 PubMed 结构化摘要与元数据撰写，付费墙全文未获取、未逐节核验，本站未做任何数值推算补全。
研究问题
No therapies exist to reverse right ventricular failure (RVF), and the molecular mechanisms that drive RVF remain understudied.
方法
We recently reported that the developmentally restricted noncanonical WNT receptor ROR2 (receptor tyrosine kinase-like orphan receptor 2) is upregulated in human RVF in proportion to severity of disease.
核心结论
Here we test the mechanistic role of ROR2 in RVF pathogenesis.；ROR2 was overexpressed or knocked down in neonatal rat ventricular myocytes and then characterized using confocal microscopy, RNA sequencing, proteomics, proteostatic functional assays, and pacing to assess contractile properties.；The impact of cardiac ROR2 expression was evaluated in mice by AAV9-mediated overexpression and by AAV9-mediated delivery of short hairpin RNA to knockdown ROR2 in a pulmonary artery banded pressure overload model of RVF.；ROR2-modified mice were evaluated by echocardiography, histology, and right ventricle protein synthesis and proteasome capacity. ‖ 结论：In sum, ROR2 is a key driver of RVF pathogenesis through proteostatic disruption and thus provides a promising target to treat RVF.
局限
未能获取全文，具体设计细节、失访与统计学处理无法核验。
对本项目的价值
★★★★★ 营养感知与自噬轴决定"干预窗口 + 剂量方案"，是组合疗法的时间锚。顶刊证据。
原文题录
- 英文标题：ROR2 Drives Right Ventricular Heart Failure Through Disruption of Proteostasis.
- 期刊与标识：Circulation · PMID 42934204 · DOI 10.1161/CIRCULATIONAHA.125.078798**
A 级证据分级：A 级（同行评议人体研究）
本文属人体研究证据，但需注意：观察性或小样本干预的结论不等于已证实临床获益；效应量与长期安全性仍需更大规模、更长随访的试验验证。
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