Interference with connective tissue growth factor attenuated fibroblast-to-myofibroblast transition and pulmonary fibrosis

Yang, Zhaohui; Wang, Mengmeng; Cao, Liping; Li, Rui; Ren, Yanping; Li, Liang; Zhang, Yuhao; Liu, Chao; Zhang, Wei; Nie, Shaoping; Sun, Zhaorui

doi:10.21037/atm-22-1397

Cited by 5 publications

(2 citation statements)

References 41 publications

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“…CTGF (CCN2) is a member of the stromal cell protein family, is a well-studied fibrosis-related factor. It is a secreted protein that is rich in cysteine and has been shown to play a crucial role in wound healing and organ fibrosis [ 108 , 109 ]. The TGF-β1/Smad/CTGF signaling pathway has been found to activate of hepatic stellate cells in a radiation-induced liver fibrosis [ 110 ].…”

Section: Mechanisms Of Radiation-induced Fibrosismentioning

confidence: 99%

Tissue fibrosis induced by radiotherapy: current understanding of the molecular mechanisms, diagnosis and therapeutic advances

Yu,

Xu,

Song

et al. 2023

J Transl Med

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Cancer remains the leading cause of death around the world. In cancer treatment, over 50% of cancer patients receive radiotherapy alone or in multimodal combinations with other therapies. One of the adverse consequences after radiation exposure is the occurrence of radiation-induced tissue fibrosis (RIF), which is characterized by the abnormal activation of myofibroblasts and the excessive accumulation of extracellular matrix. This phenotype can manifest in multiple organs, such as lung, skin, liver and kidney. In-depth studies on the mechanisms of radiation-induced fibrosis have shown that a variety of extracellular signals such as immune cells and abnormal release of cytokines, and intracellular signals such as cGAS/STING, oxidative stress response, metabolic reprogramming and proteasome pathway activation are involved in the activation of myofibroblasts. Tissue fibrosis is extremely harmful to patients' health and requires early diagnosis. In addition to traditional serum markers, histologic and imaging tests, the diagnostic potential of nuclear medicine techniques is emerging. Anti-inflammatory and antioxidant therapies are the traditional treatments for radiation-induced fibrosis. Recently, some promising therapeutic strategies have emerged, such as stem cell therapy and targeted therapies. However, incomplete knowledge of the mechanisms hinders the treatment of this disease. Here, we also highlight the potential mechanistic, diagnostic and therapeutic directions of radiation-induced fibrosis.

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Section: Mechanisms Of Radiation-induced Fibrosismentioning

confidence: 99%

Tissue fibrosis induced by radiotherapy: current understanding of the molecular mechanisms, diagnosis and therapeutic advances

Yu,

Xu,

Song

et al. 2023

J Transl Med

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“…As before, we still verified at the cellular level. Excessive deposition of the ECM is one of the important causes of fibrotic phenotype 34 . We overexpressed or knocked down the JMJD3 protein and re-examined the expression of fibrotic proteins by Western blot in LPS-induced hBSMCs, including α-SMA, a recognized marker of myofibroblast activation.…”

Section: Emodin Inhibits Bladder Fibrosis and Extracellular Matrix De...mentioning

confidence: 99%

Emodin inhibits bladder inflammation and fibrosis in mice with interstitial cystitis by regulating JMJD3

Lai,

Liu,

et al. 2023

Acta Cir. Bras.

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Interstitial cystitis/bladder pain syndrome (IC/BPS) is a devastating urological chronic pelvic pain condition. In search of a potential treatment, we investigated the effect of emodin on IC/BPS inflammation and fibrosis, and explore the potential mechanism. Methods: An experimental model of interstitial cystitis was induced by cyclophosphamide, and human bladder smooth muscle cells were treated with lipopolysaccharide to establish the cell model in vitro. In both models, inflammation-and fibrosis-related indexes were measured after emodin administration. Furthermore, the specific antagonists were used to dig for the mechanisms underlying the response to emodin treatment. Results: Emodin significantly ameliorated management of cystitis, reduced the amount of inflammatory cytokines (tumor necrosis factor-α, monocyte chemoattractant protein-1, interleukin-1β, interleukin-8, and interleukin-6) in models, as well as reducing the synthesis of fibrosis marker including collagen1, collagen3, vimentin, fibronectin and α-smooth muscle actin. Further mechanism studies demonstrated that emodin inhibited inflammatory reaction and fibrosis through blocking lysine-specific demethylase 6B (JMJD3) expression via JAK/STAT, NF-κB and TGF-β/SMAD pathways. Conclusion: Our study reveals the critical role of emodin-JMJD3 signaling in interstitial cystitis by regulating inflammation, fibrosis, and extracellular matrix deposition in cells and tissues, and these findings provide an avenue for effective treatment of patients with cystitis.

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Piceatannol-mediated JAK2/STAT3 signaling pathway inhibition contributes to the alleviation of oxidative injury and collagen synthesis during pulmonary fibrosis

Tong

Ying²,

Zhang³

et al. 2022

International Immunopharmacology

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Interference with connective tissue growth factor attenuated fibroblast-to-myofibroblast transition and pulmonary fibrosis

Cited by 5 publications

References 41 publications

Tissue fibrosis induced by radiotherapy: current understanding of the molecular mechanisms, diagnosis and therapeutic advances

Tissue fibrosis induced by radiotherapy: current understanding of the molecular mechanisms, diagnosis and therapeutic advances

Emodin inhibits bladder inflammation and fibrosis in mice with interstitial cystitis by regulating JMJD3

Piceatannol-mediated JAK2/STAT3 signaling pathway inhibition contributes to the alleviation of oxidative injury and collagen synthesis during pulmonary fibrosis

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