Irreversibility of Pulmonary Fibrosis

Yu, Qing; Tang, Xiao Xiao

doi:10.14336/ad.2021.0730

Cited by 41 publications

(23 citation statements)

References 123 publications

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“…In the pathological produce of pulmonary fibrosis, alveolitis comes first, then the fibroblast is activated, expressed FAP, and then activated fibroblast differentiate to myofibroblast, which is a key cell-expressed α-SMA to produce excessive exocellular matrix ( Yu and Tang, 2022 ). The excessive exocellular matrix is comprised of collagen fibers, which can be determined by Masson staining and FN IHC.…”

Section: Resultsmentioning

confidence: 99%

Mesoporous Polydopamine Loaded Pirfenidone Target to Fibroblast Activation Protein for Pulmonary Fibrosis Therapy

Fang

Liu

Cui

et al. 2022

Front. Bioeng. Biotechnol.

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Recently, fibroblast activation protein (FAP), an overexpressed transmembrane protein of activated fibroblast in pulmonary fibrosis, has been considered as the new target for diagnosing and treating pulmonary fibrosis. In this work, mesoporous polydopamine (MPDA), which is facile prepared and easily modified, is developed as a carrier to load antifibrosis drug pirfenidone (PFD) and linking FAP inhibitor (FAPI) to realize lesion-targeted drug delivery for pulmonary fibrosis therapy. We have found that PFD@MPDA-FAPI is well biocompatible and with good properties of antifibrosis, when ICG labels MPDA-FAPI, the accumulation of the nanodrug at the fibrosis lung in vivo can be observed by NIR imaging, and the antifibrosis properties of PFD@MPDA-FAPI in vivo were also better than those of pure PFD and PFD@MPDA; therefore, the easily produced and biocompatible nanodrug PFD@MPDA-FAPI developed in this study is promising for further clinical translations in pulmonary fibrosis antifibrosis therapy.

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Section: Resultsmentioning

confidence: 99%

Mesoporous Polydopamine Loaded Pirfenidone Target to Fibroblast Activation Protein for Pulmonary Fibrosis Therapy

Fang

Liu

Cui

et al. 2022

Front. Bioeng. Biotechnol.

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“…Similar to the liver, kidney, and other organs, endometrial fibrosis is also a scar formation process. On the one hand, it is related to an increase in ECM deposition [ 34 ]. On the other hand, ESCs can be transformed into myofibroblasts under stimulation with TGF-β1 and participate in endometrial fibrosis [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

β-Klotho Promotes the Development of Intrauterine Adhesions via the PI3K/AKT Signaling Pathway

Guo

Wang

Wen

et al. 2022

IJMS

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Intrauterine adhesion (IUA) refers to injury to the basal layer of the endometrium, which can be caused by various factors. It is often accompanied by clinical symptoms such as abnormal menstruation, infertility, recurrent abortion, and periodic abdominal pain. In recent years, a number of studies have reported the effects of β-Klotho (KLB) on the occurrence and development of human tumors and fibrotic diseases, but its relationship with endometrial fibroblasts and endometrial fibrosis has not been elucidated. In this study, we compared the expression of KLB in endometrial stromal cells (ESCs) from patients with IUA and normal controls. We constructed animal and cell models of IUA and conducted expression verification and functional experiments on KLB. We found that the expression of KLB was significantly increased in the ESCs of IUA patients and rat models compared with the controls. The overexpression of KLB could promote the proliferation and fibrosis of ESCs. In addition, the overexpression of KLB activated the PI3K/AKT signaling pathway in ESCs. Our study shows that KLB protein is highly expressed in the ESCs of patients with IUA and can enhance stromal cell proliferation and cell fibrosis by activating the PI3K/AKT pathway, thus promoting the development of IUA.

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“…Pulmonary fibrosis is the consequence of aberrant wound healing, which results in a cascade of pathological changes that replaces the lung parenchyma with an extracellular matrix ( 60 ). On imaging, pulmonary fibrosis is suggested by the parenchymal bands, reticular opacities, traction bronchiectasis, and honeycombing ( 61 ).…”

Section: Post-covid-19 Lung Fibrosismentioning

confidence: 99%

Cardiopulmonary disease as sequelae of long-term COVID-19: Current perspectives and challenges

et al. 2022

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COVID-19 infection primarily targets the lungs, which in severe cases progresses to cytokine storm, acute respiratory distress syndrome, multiorgan dysfunction, and shock. Survivors are now presenting evidence of cardiopulmonary sequelae such as persistent right ventricular dysfunction, chronic thrombosis, lung fibrosis, and pulmonary hypertension. This review will summarize the current knowledge on long-term cardiopulmonary sequelae of COVID-19 and provide a framework for approaching the diagnosis and management of these entities. We will also identify research priorities to address areas of uncertainty and improve the quality of care provided to these patients.

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Irreversibility of Pulmonary Fibrosis

Cited by 41 publications

References 123 publications

Mesoporous Polydopamine Loaded Pirfenidone Target to Fibroblast Activation Protein for Pulmonary Fibrosis Therapy

Mesoporous Polydopamine Loaded Pirfenidone Target to Fibroblast Activation Protein for Pulmonary Fibrosis Therapy

β-Klotho Promotes the Development of Intrauterine Adhesions via the PI3K/AKT Signaling Pathway

Cardiopulmonary disease as sequelae of long-term COVID-19: Current perspectives and challenges

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