Dihydroergotamine ameliorates liver fibrosis by targeting transforming growth factor β type II receptor

Zheng, Kexin; Yuan, Shouli; Dong, Meng; Zhang, Hanlin; Jiang, Xiaoxiao; Yan, Chunlong; Ye, Rongcai; Zhou, Huiqiao; Chen, Li; Jiang, Rui; Cheng, Zhenguo; Zhang, Zhi; Wang, Qi; Jin, Wanzhu; Xie, Wen

doi:10.3748/wjg.v29.i20.3103

Cited by 3 publications

(2 citation statements)

References 41 publications

(47 reference statements)

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“…( FNDC3A , COL7A1 , MMP9 ) [ 44 , 45 ], at 32 h p.i. ( TGFβR2 , COL13A1 , MMP16 ) [ 46 , 47 ] or at both time points ( PLAUR , TGFβ1 , TGFβ3 ) [ 48 , 49 , 50 ]. Among a set of selected and highly regulated DEGs involved in the different stages of the fibrotic process, PLAUR , TGFβ1 and FOSB evidenced their potential as relevant biomarkers of disease progression in the scrotal skin of naturally infected bulls.…”

Section: Discussionmentioning

confidence: 99%

Transcriptomics of Besnoitia besnoiti-Infected Fibroblasts Reveals Hallmarks of Early Fibrosis and Cancer Progression

Fernández-Álvarez,

Horcajo,

Jiménez-Meléndez

et al. 2024

Microorganisms

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Endothelial injury, inflammatory infiltrate and fibrosis are the predominant lesions in the testis of bulls with besnoitiosis that may result in sterility. Moreover, fibroblasts, which are key players in fibrosis, are parasite target cells in a Besnoitia besnoiti chronic infection. This study aimed to decipher the molecular basis that underlies a drift toward fibrosis during the disease progression. Transcriptomic analysis was developed at two times post-infection (p.i.), representative of invasion (12 h p.i.) and intracellular proliferation (32 h p.i.), in primary bovine aorta fibroblasts infected with B. besnoiti tachyzoites. Once the enriched host pathways were identified, we studied the expression of selected differentially expressed genes (DEGs) in the scrotal skin of sterile infected bulls. Functional enrichment analyses of DEGs revealed shared hallmarks of cancer and early fibrosis. Biomarkers of inflammation, angiogenesis, cancer, and MAPK signaling stood out at 12 h p.i. At 32 h p.i., again MAPK and cancer pathways were enriched together with the PI3K–AKT pathway related to cell proliferation. Some DEGs were also regulated in the skin samples of naturally infected bulls (PLAUR, TGFβ1, FOSB). We have identified potential biomarkers and host pathways regulated during fibrosis that may hold prognostic significance and could emerge as potential therapeutic targets.

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Section: Discussionmentioning

confidence: 99%

Transcriptomics of Besnoitia besnoiti-Infected Fibroblasts Reveals Hallmarks of Early Fibrosis and Cancer Progression

Fernández-Álvarez,

Horcajo,

Jiménez-Meléndez

et al. 2024

Microorganisms

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“…Liver fibrosis is the result of excessive extracellular matrix (ECM) deposition after liver injury, and it can lead to cirrhosis and hepatocellular carcinoma[ 8 ]. In essence, liver fibrosis is a response to repeated wound repair after continuous liver tissue damage.…”

Section: Tgf-β and Hepatic Fibrosismentioning

confidence: 99%

Roles of transforming growth factor-β signaling in liver disease

Wang,

Yang,

Wang

2024

World J Hepatol

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In this editorial we expand the discussion on the article by Zhang et al published in the recent issue of the World Journal of Hepatology . We focus on the diagnostic and therapeutic targets identified on the basis of the current understanding of the molecular mechanisms of liver disease. Transforming growth factor-β (TGF-β) belongs to a structurally related cytokine super family. The family members display different time- and tissue-specific expression patterns associated with autoimmunity, inflammation, fibrosis, and tumorigenesis; and, they participate in the pathogenesis of many diseases. TGF-β and its related signaling pathways have been shown to participate in the progression of liver diseases, such as injury, inflammation, fibrosis, cirrhosis, and cancer. The often studied TGF-β/Smad signaling pathway has been shown to promote or inhibit liver fibrosis under different circumstances. Similarly, the early immature TGF-β molecule functions as a tumor suppressor, inducing apoptosis; but, its interaction with the mitogenic molecule epidermal growth factor alters this effect, activating anti-apoptotic signals that promote liver cancer development. Overall, TGF-β signaling displays contradictory effects in different liver disease stages. Therefore, the use of TGF-β and related signaling pathway molecules for diagnosis and treatment of liver diseases remains a challenge and needs further study. In this editorial, we aim to review the evidence for the use of TGF-β signaling pathway molecules as diagnostic or therapeutic targets for different liver disease stages.

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Exosomes from adipose-derived mesenchymal stem cells improve liver fibrosis by regulating the miR-20a-5p/TGFBR2 axis to affect the p38 MAPK/NF-κB pathway

Gan,

Zheng,

Yao

et al. 2023

Cytokine

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Dihydroergotamine ameliorates liver fibrosis by targeting transforming growth factor β type II receptor

Cited by 3 publications

References 41 publications

Transcriptomics of Besnoitia besnoiti-Infected Fibroblasts Reveals Hallmarks of Early Fibrosis and Cancer Progression

Transcriptomics of Besnoitia besnoiti-Infected Fibroblasts Reveals Hallmarks of Early Fibrosis and Cancer Progression

Roles of transforming growth factor-β signaling in liver disease

Exosomes from adipose-derived mesenchymal stem cells improve liver fibrosis by regulating the miR-20a-5p/TGFBR2 axis to affect the p38 MAPK/NF-κB pathway

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