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肾纤维化分子机制:Spp1通过转化生长因子β-Smad信号通路影响成纤维细胞活性。

Kidney fibrosis molecular mechanisms Spp1 influences fibroblast activity through transforming growth factor beta smad signaling.

作者信息

Ding Hao, Xu Zidu, Lu Ying, Yuan Qi, Li Jianzhong, Sun Qi

机构信息

Center for Kidney Disease, Second Affiliated Hospital of Nanjing Medical University, Nanjing 210000, P.R. China.

Emergency Medicine Center, Second Affiliated Hospital of Nanjing Medical University, Nanjing 210000, P.R. China.

出版信息

iScience. 2024 May 9;27(9):109839. doi: 10.1016/j.isci.2024.109839. eCollection 2024 Sep 20.

DOI:10.1016/j.isci.2024.109839
PMID:39323737
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11422156/
Abstract

Kidney fibrosis marks a critical phase in chronic kidney disease with its molecular intricacies yet to be fully understood. This study's deep dive into single-cell sequencing data of renal tissue during fibrosis pinpoints the pivotal role of fibroblasts and myofibroblasts in the fibrotic transformation. Through identifying distinct cell populations and conducting transcriptomic analysis, Spp1 emerged as a key gene associated with renal fibrosis. The study's experimental findings further confirm Spp1's vital function in promoting fibroblast to myofibroblast differentiation via the TGF-β/Smad signaling pathway, underscoring its contribution to fibrosis progression. The suppression of Spp1 expression notably hindered this differentiation process, spotlighting Spp1 as a promising therapeutic target for halting renal fibrosis. This condensed summary encapsulates the essence and findings of the original research within the specified word limit.

摘要

肾纤维化是慢性肾脏病的一个关键阶段,其分子复杂性尚未完全明了。本研究深入探究纤维化过程中肾组织的单细胞测序数据,明确了成纤维细胞和平滑肌肌动蛋白阳性成纤维细胞在纤维化转变中的关键作用。通过识别不同的细胞群体并进行转录组分析,分泌磷蛋白1(Spp1)成为与肾纤维化相关的关键基因。该研究的实验结果进一步证实,Spp1通过转化生长因子-β/信号转导和转录激活因子(TGF-β/Smad)信号通路在促进成纤维细胞向平滑肌肌动蛋白阳性成纤维细胞分化中发挥重要作用,突出了其对纤维化进展的作用。抑制Spp1表达显著阻碍了这一分化过程,使Spp1成为阻止肾纤维化的一个有前景的治疗靶点。这一简要总结在规定字数范围内概括了原始研究的精髓和结果。

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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c89d/11422156/1e29ddfd5967/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c89d/11422156/e2e7b25393f5/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c89d/11422156/f811ab92fb51/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c89d/11422156/754b297d8ad6/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c89d/11422156/aaa8732eed6d/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c89d/11422156/86f6e2574758/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c89d/11422156/c4b042d6b0d6/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c89d/11422156/19fdecced024/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c89d/11422156/a9bb2417b52c/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c89d/11422156/b91ff20562c4/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c89d/11422156/cba946d068fe/gr10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c89d/11422156/ae1e25ea4f01/gr11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c89d/11422156/53809a3f9805/gr12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c89d/11422156/23fe4c82b2ee/gr13.jpg

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