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首页> 外文期刊>Genomics >Transition from compensated hypertrophy to systolic heart failure in the spontaneously hypertensive rat: Structure, function, and transcript analysis
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Transition from compensated hypertrophy to systolic heart failure in the spontaneously hypertensive rat: Structure, function, and transcript analysis

机译：自发性高血压大鼠从代偿性肥大到收缩性心力衰竭的转变：结构，功能和转录本分析

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Gene expression, determined by micro-array analysis, and left ventricular (LV) remodeling associated with the transition to systolic heart failure (HF) were examined in the spontaneously hypertensive rat (SHR). By combining transcript and gene set enrichment analysis (GSEA) of the LV with assessment of function and structure in age-matched SHR with and without HF, we aimed to better understand the molecular events underlying the onset of hypertensive HF. Failing hearts demonstrated depressed LV ejection fraction, systolic blood pressure, and LV papillary muscle force while LV end-diastolic and systolic volume and ventricular mass increased. 1431 transcripts were differentially expressed between failing and non-failing animals. GSEA identified multiple enriched gene sets, including those involving inflammation, oxidative stress, cell degradation and cell death, as well as TGF-β and insulin signaling pathways. Our findings support the concept that these pathways and mechanisms may contribute to deterioration of cardiac function and remodeling associated with hypertensive HF.
机译：在自发性高血压大鼠（SHR）中检查了通过微阵列分析确定的基因表达，以及与向收缩性心力衰竭（HF）过渡相关的左心室（LV）重塑。通过结合LV的转录本和基因集富集分析（GSEA），以及在有或没有HF的年龄匹配的SHR中评估功能和结构，我们旨在更好地了解高血压HF发作的分子事件。衰竭的心脏表现出左室射血分数，收缩压和左室乳头肌力降低，而左室舒张末期和收缩期容积以及心室质量增加。在失败和未失败的动物之间差异表达了1431个转录物。 GSEA鉴定了多种富集的基因集，包括那些涉及炎症，氧化应激，细胞降解和细胞死亡以及TGF-β和胰岛素信号通路的基因集。我们的发现支持以下观念：这些途径和机制可能会导致与高血压性心衰相关的心脏功能恶化和重塑。

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