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Updated: Feb 28, 2026

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WISP1驱动了一种机械活跃的免疫调节和增殖的心脏肌纤维细胞状态

Sharon Parkins, Sarah R Anthony, Teagan K Goldsworthy

bioRxiv : the preprint server for biology

|February 27, 2026

概括

母细胞蛋白WISP1通过独特的途径驱动心肌纤维细胞活性,促进增殖和免疫调节,而不是传统的纤维化. 这一发现为病态心脏重塑提供了新的见解.

科学领域:

心血管生物学心血管生物学
纤维化研究纤维化研究
细胞信号传递细胞信号传递

背景情况:

病理性心脏重塑涉及纤维细胞到肌纤维细胞的分化和过度的细胞外基质 (ECM) 沉积,导致组织硬化.
母细胞蛋白WISP1在心脏纤维化时被上调,并促进肌纤维细胞活性,但其精确的机制尚不清楚.

研究的目的:

研究WISP1在驱动心脏肌纤维细胞活动中的功能作用和潜在机制.
为了确定WISP1是否诱导独特或正规的肌纤维细胞表型.

主要方法:

成年小鼠的初级心脏纤维细胞被用WISP1和/或TGFβ1.1治疗.
评估了肌纤维细胞标记物 (α-SMA,原I,环素),ECM分泌物,收缩性和伤口愈合.
利用P38 MAPK抑制和多omics方法 (RNA-seq,蛋白质组) 来定义WISP1的影响.

主要成果:

不管性别,WISP1显著增加了α-SMA,原I表达,分泌和纤维细胞收缩性.
单独的WISP1并没有诱导皮奥斯,这表明它具有独特的表型,并且通过非正规的P38 MAPK通路调解活性.
多种omics揭示WISP1广泛促进增殖和免疫调节基因/蛋白质表达,与TGFβ1.1的上下文依赖的相互作用.

结论:

WISP1促进一种独特的增殖和免疫调节的肌纤维细胞表型,与公认的TGFβ1驱动纤维化不同.
WISP1的活动通过非正规的P38 MAPK依赖的信号通路进行介导.
这些发现阐明了心脏重塑中的新机制,并建议WISP1作为潜在的治疗点.

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