数据日期 2026-10-29 · 生成时间 2026-10-29 06:03
研究问题
Ischemic and nonischemic heart disease arise from different initiating injuries but can progress toward shared end-stage myocardial remodeling [1,2].
方法
Human heart tissue samples were obtained from a deidentified cardiac tissue collection established through the long-standing collaboration between Dr.;The collection included failing human left-ventricular myocardium obtained at the time of cardiac transplantation or mechanical circulatory support, as well as nonfailing donor hearts that were unsuitable for transplantation.;The final analysis included 75 samples (20 female and 55 male) after exclusion of one likely duplicate sample.;Samples were processed in two batches, and batch was included in the differential-expression models.
核心结论
At 80% power and a two-sided α of 0.05, the median minimum detectable effect across expressed genes was an absolute log2 fold change of 0.465, corresponding to approximately a 1.38-fold difference.;The interquartile range was 0.256–0.938 in absolute log2 fold change, corresponding to approximately 1.19- to 1.92-fold differences. ‖ 结论:These etiology-associated differences should be considered exploratory because they did not remain significant after FDR correction.
局限
Nominal findings from the direct disease, sex, and race comparisons should be considered hypothesis-generating and require further replication.;Although batch was included as a covariate and the Batch-1-only sensitivity analysis showed substantial directional concordance with the full batch-adjusted analyses, the unbalanced design may limit complete separation of technical and biological effects.
对本项目的价值
★★☆☆☆ 血管老化提供可影像量化、可短期读取的中间终点,适合做机制到临床的桥接。最大样本量约 10;设计 多组学。
全文来源
PMC JATS 全文(正文 34,475 字符,已过标题/DOI 逐字归属校验)
原文题录
- 英文标题:Immune-Inflammatory, Autophagy, and JNK Remodeling in Ischemic and Nonischemic Human Myocardium.
- 期刊与标识:Curr Issues Mol Biol · PMID 42939620 · DOI 10.3390/cimb48101082**
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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