Cigarette smoking aggravates bleomycin-induced experimental pulmonary fibrosis

Zhou, Linlin; Wang, Meng; Liu, Fei; Lu, Yang; Song, Linjie; Xiong, Liang; Fei, Xiang; He, Xiaowen; Shuai, Shi-Yuan; Xin, Jian-Bao; Hong, Yan; Fan, Yu; Ma, Wanli

doi:10.1016/j.toxlet.2018.12.008

Cited by 26 publications

(21 citation statements)

References 33 publications

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“…In vitro cigarette smoke extract (CSE) treatment in lung fibroblasts induced p-Smad2/3 and p-AKT as well as collagen synthesis [90]. This treatment further enhanced TGF-β1 mediated p-Smad2/3 and p-AKT signaling pathways in the lungs of bleomycin-treated mice [90] (Fig. 1).…”

Section: Metabolic Reprogramming and Collagen Productionmentioning

confidence: 92%

“…It was suggested that CS exposure created a profibrotic milieu to further potentiate the bleomycin-induced lung fibrosis [89]. In vitro cigarette smoke extract (CSE) treatment in lung fibroblasts induced p-Smad2/3 and p-AKT as well as collagen synthesis [90]. This treatment further enhanced TGF-β1 mediated p-Smad2/3 and p-AKT signaling pathways in the lungs of bleomycin-treated mice [90] (Fig.…”

Section: Metabolic Reprogramming and Collagen Productionmentioning

confidence: 99%

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Metabolic reprogramming: A driver of cigarette smoke-induced inflammatory lung diseases

Yang

Chen

2021

Free Radical Biology and Medicine

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Cigarette smoking is a well-known risk factor for pulmonary diseases, including chronic obstructive pulmonary disease (COPD), asthma and pulmonary fibrosis. Despite major progress in dissecting the mechanisms associated with disease development and progression, findings only represent one aspect of multifaceted disease. A crucial consequence of this approach is that many therapeutic treatments often fail to improve or reverse the disease state as other conditions and variables are insufficiently considered. To expand our understanding of pulmonary diseases, omics approaches, particularly metabolomics, has been emerging in the field. This strategy has been applied to identify putative biomarkers and novel mechanistic insights. In this review, we discuss metabolic profiles of patients with COPD, asthma, and idiopathic pulmonary fibrosis (IPF) with a focus on the direct effects of cigarette smoking in altering metabolic regulation. We next present cell-and animal-based experiments and point out the therapeutic potential of targeting metabolic reprogramming in inflammatory lung diseases. In addition, the obstacles in translating these findings into clinical practice, including potential adverse effects and limited pharmacological efficacy, are also addressed.

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Section: Metabolic Reprogramming and Collagen Productionmentioning

confidence: 92%

Section: Metabolic Reprogramming and Collagen Productionmentioning

confidence: 99%

Metabolic reprogramming: A driver of cigarette smoke-induced inflammatory lung diseases

Yang

Chen

2021

Free Radical Biology and Medicine

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“…Transforming growth factor-β1 (TGF-β1) serves as a multifunctional cellular regulator. Following activation of TGF-β1, activated TGF-β1 binds to its receptor and activates downstream Smad signalling, including Smad2 and Smad3, which serves a crucial role in tissue fibrosis (6,7), including cardiac (8), liver (9), pulmonary (10), pancreatic (11) and renal fibrosis (12), and chronic autoimmune disease Sjögren's syndrome (SS) (13). The mechanism of the TGF-β1/Smad signalling pathway involved in the occurrence of intrauterine adhesions has been described previously (14,15).…”

Section: Introductionmentioning

confidence: 99%

Aspirin inhibits endometrial fibrosis by suppressing the�TGF‑β1‑Smad2/Smad3 pathway in intrauterine adhesions

Zhang

Deng

et al. 2020

Int J Mol Med

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Intrauterine adhesions (IUAs) represent one of the most common diseases in women of reproductive age. Patients with moderate-to-severe IUA can experience a decrease in normal menstrual patterns, amenorrhea and even infertility. At present, the first-line treatment strategies for IUAs in the clinical practice are hysteroscopic transuterine resection of adhesion and postoperative adjuvant therapy, including oestrogen. However, a high recurrence rate of IUAs remains.

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“…A study reported that CS aggravates bleomycin-induced pulmonary fibrosis via TGF-β1 signaling, but necroptosis was not mentioned (Zhou et al, 2019). It will be interesting to explore the function of necroptosis in CS-related pulmonary fibrosis and determine if CS-induced necroptosis leads to IPF or COPD.…”

Section: Idiopathic Pulmonary Fibrosismentioning

confidence: 99%

“…Interestingly, IPF and COPD have a lot in common in terms of pathogenesis, including their relationship with smoking, lung aging biopathological processes ( Duckworth et al, 2021 ; Schuliga et al, 2021 ) and necroptosis-involved pathological mechanisms. A study reported that CS aggravates bleomycin-induced pulmonary fibrosis via TGF-β1 signaling, but necroptosis was not mentioned ( Zhou et al, 2019 ). It will be interesting to explore the function of necroptosis in CS-related pulmonary fibrosis and determine if CS-induced necroptosis leads to IPF or COPD.…”

Section: The Role Of Necroptosis In Lung Diseasesmentioning

confidence: 99%

Necroptosis in Pulmonary Diseases: A New Therapeutic Target

Wang

Zhou

et al. 2021

Front. Pharmacol.

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In the past decades, apoptosis has been the most well-studied regulated cell death (RCD) that has essential functions in tissue homeostasis throughout life. However, a novel form of RCD called necroptosis, which requires receptor-interacting protein kinase-3 (RIPK3) and mixed-lineage kinase domain-like pseudokinase (MLKL), has recently been receiving increasing scientific attention. The phosphorylation of RIPK3 enables the recruitment and phosphorylation of MLKL, which oligomerizes and translocates to the plasma membranes, ultimately leading to plasma membrane rupture and cell death. Although apoptosis elicits no inflammatory responses, necroptosis triggers inflammation or causes an innate immune response to protect the body through the release of damage-associated molecular patterns (DAMPs). Increasing evidence now suggests that necroptosis is implicated in the pathogenesis of several human diseases such as systemic inflammation, respiratory diseases, cardiovascular diseases, neurodegenerative diseases, neurological diseases, and cancer. This review summarizes the emerging insights of necroptosis and its contribution toward the pathogenesis of lung diseases.

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Cigarette smoking aggravates bleomycin-induced experimental pulmonary fibrosis

Cited by 26 publications

References 33 publications

Metabolic reprogramming: A driver of cigarette smoke-induced inflammatory lung diseases

Metabolic reprogramming: A driver of cigarette smoke-induced inflammatory lung diseases

Aspirin inhibits endometrial fibrosis by suppressing the�TGF‑β1‑Smad2/Smad3 pathway in intrauterine adhesions

Necroptosis in Pulmonary Diseases: A New Therapeutic Target

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