Cellular Interactions and Crosstalk Facilitating Biliary Fibrosis in Cholestasis

IF 7.1 1区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Cellular and Molecular Gastroenterology and Hepatology Pub Date : 2024-01-01 DOI:10.1016/j.jcmgh.2024.01.005

Ludovica Ceci , Eugenio Gaudio , Lindsey Kennedy

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引用次数: 0

Abstract

Biliary fibrosis is seen in cholangiopathies, including primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PSC). In PBC and PSC, biliary fibrosis is associated with worse outcomes and histologic scores. Within the liver, both hepatic stellate cells (HSCs) and portal fibroblasts (PFs) contribute to biliary fibrosis, but their roles can differ. PFs reside near the bile ducts and may be the first responders to biliary damage, whereas HSCs may be recruited later and initiate bridging fibrosis. Indeed, different models of biliary fibrosis can activate PFs and HSCs to varying degrees. The portal niche can be composed of cholangiocytes, HSCs, PFs, endothelial cells, and various immune cells, and interactions between these cell types drive biliary fibrosis. In this review, we discuss the mechanisms of biliary fibrosis and the roles of PFs and HSCs in this process. We will also evaluate cellular interactions and mechanisms that contribute to biliary fibrosis in different models and highlight future perspectives and potential therapeutics.

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胆汁淤积症中促进胆汁纤维化的细胞相互作用和相互影响

胆道纤维化见于胆道疾病，包括原发性胆汁性胆管炎（PBC）和原发性硬化性胆管炎（PSC）。在原发性胆汁性胆管炎和原发性硬化性胆管炎中，胆汁纤维化与较差的预后和组织学评分有关。在肝脏内，肝星状细胞（HSCs）和肝门成纤维细胞（PFs）都会导致胆道纤维化，但它们的作用可能有所不同。门叶成纤维细胞位于胆管附近，可能是胆道损伤的第一反应者，而造血干细胞则可能在较晚的时候被招募并引发桥接性纤维化。事实上，不同的胆道纤维化模型可在不同程度上激活胆道干细胞和造血干细胞。门户龛可由胆管细胞、造血干细胞、PFs、内皮细胞和各种免疫细胞组成，这些细胞类型之间的相互作用推动了胆道纤维化。在本综述中，我们将讨论胆道纤维化的机制以及胆道干细胞和造血干细胞在这一过程中的作用。我们还将评估不同模型中导致胆道纤维化的细胞相互作用和机制，并强调未来前景和潜在疗法。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cellular and Molecular Gastroenterology and Hepatology Medicine-Gastroenterology

CiteScore

13.00

自引率

2.80%

发文量

246

审稿时长

42 days

期刊介绍： "Cell and Molecular Gastroenterology and Hepatology (CMGH)" is a journal dedicated to advancing the understanding of digestive biology through impactful research that spans the spectrum of normal gastrointestinal, hepatic, and pancreatic functions, as well as their pathologies. The journal's mission is to publish high-quality, hypothesis-driven studies that offer mechanistic novelty and are methodologically robust, covering a wide range of themes in gastroenterology, hepatology, and pancreatology. CMGH reports on the latest scientific advances in cell biology, immunology, physiology, microbiology, genetics, and neurobiology related to gastrointestinal, hepatobiliary, and pancreatic health and disease. The research published in CMGH is designed to address significant questions in the field, utilizing a variety of experimental approaches, including in vitro models, patient-derived tissues or cells, and animal models. This multifaceted approach enables the journal to contribute to both fundamental discoveries and their translation into clinical applications, ultimately aiming to improve patient care and treatment outcomes in digestive health.