Impact of Depression on Patients With Idiopathic Pulmonary Fibrosis

Τzouvelekis, Αrgyris; Karampitsakos, Theodoros; Kourtidou, Sofia; Bouros, Evangelos; Tzilas, Vasilios; Katsaras, Matthaios; Antonou, Chrysoula; Dassiou, M; Bouros, Demosthenes

doi:10.3389/fmed.2020.00029

Cited by 30 publications

(16 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…1a ). Then, we assessed the correlation between the levels of ACP5 and disease severity, which were estimated by the lung’s gas diffusing capacity 20 (as measured by the diffusing capacity of the lungs for carbonmonoxide, DLCO). Notably, the levels of ACP5 were higher in severe IPF patients whose DLCO were less than 40% of the predicted value than in patients with less severe IPF (Fig.…”

Section: Resultsmentioning

confidence: 99%

Tartrate-resistant acid phosphatase 5 promotes pulmonary fibrosis by modulating β-catenin signaling

Wang

et al. 2022

Nat Commun

View full text Add to dashboard Cite

Idiopathic pulmonary fibrosis (IPF) is a fatal interstitial lung disease with limited therapeutic options. Tartrate-resistant acid phosphatase 5 (ACP5) performs a variety of functions. However, its role in IPF remains unclear. Here, we demonstrate that the levels of ACP5 are increased in IPF patient samples and mice with bleomycin (BLM)-induced pulmonary fibrosis. In particular, higher levels of ACP5 are present in the sera of IPF patients with a diffusing capacity of the lungs for carbonmonoxide (DLCO) less than 40% of the predicted value. Additionally, Acp5 deficiency protects mice from BLM-induced lung injury and fibrosis coupled with a significant reduction of fibroblast differentiation and proliferation. Mechanistic studies reveal that Acp5 is upregulated by transforming growth factor-β1 (TGF-β1) in a TGF-β receptor 1 (TGFβR1)/Smad family member 3 (Smad3)-dependent manner, after which Acp5 dephosphorylates p-β-catenin at serine 33 and threonine 41, inhibiting the degradation of β-catenin and subsequently enhancing β-catenin signaling in the nucleus, which promotes the differentiation, proliferation and migration of fibroblast. More importantly, the treatment of mice with Acp5 siRNA-loaded liposomes or Acp5 inhibitor reverses established lung fibrosis. In conclusions, Acp5 is involved in the initiation and progression of pulmonary fibrosis and strategies aimed at silencing or suppressing Acp5 could be considered as potential therapeutic approaches against pulmonary fibrosis.

show abstract

Section: Resultsmentioning

confidence: 99%

Tartrate-resistant acid phosphatase 5 promotes pulmonary fibrosis by modulating β-catenin signaling

Wang

et al. 2022

Nat Commun

View full text Add to dashboard Cite

show abstract

“…Our study suggested that the model provided almost instantaneous reporting with accuracy and reproducibility comparable to human experts (AUC 0.96 vs 0.91 in test set 1, AUC 0.92 vs 0.81 in test set 2). As a fatal complication of IPF, the accurate classification of AE-IPF plays a crucial role in improving prognostication, directing patient treatment and facilitating research 25–27. AE-IPF shares similar pathophysiological characteristics with acute respiratory distress syndrome, which can be triggered by COVID-19 and is considered one of the major causes of increased mortality 28 29.…”

Section: Discussionmentioning

confidence: 99%

Novel 3D-based deep learning for classification of acute exacerbation of idiopathic pulmonary fibrosis using high-resolution CT

Huang,

Si,

et al. 2024

BMJ Open Resp Res

View full text Add to dashboard Cite

PurposeAcute exacerbation of idiopathic pulmonary fibrosis (AE-IPF) is the primary cause of death in patients with IPF, characterised by diffuse, bilateral ground-glass opacification on high-resolution CT (HRCT). This study proposes a three-dimensional (3D)-based deep learning algorithm for classifying AE-IPF using HRCT images.Materials and methodsA novel 3D-based deep learning algorithm, SlowFast, was developed by applying a database of 306 HRCT scans obtained from two centres. The scans were divided into four separate subsets (training set, n=105; internal validation set, n=26; temporal test set 1, n=79; and geographical test set 2, n=96). The final training data set consisted of 1050 samples with 33 600 images for algorithm training. Algorithm performance was evaluated using accuracy, sensitivity, specificity, positive predictive value, negative predictive value, receiver operating characteristic (ROC) curve and weighted κ coefficient.ResultsThe accuracy of the algorithm in classifying AE-IPF on the test sets 1 and 2 was 93.9% and 86.5%, respectively. Interobserver agreements between the algorithm and the majority opinion of the radiologists were good (κw=0.90 for test set 1 and κw=0.73 for test set 2, respectively). The ROC accuracy of the algorithm for classifying AE-IPF on the test sets 1 and 2 was 0.96 and 0.92, respectively. The algorithm performance was superior to visual analysis in accurately diagnosing radiological findings. Furthermore, the algorithm’s categorisation was a significant predictor of IPF progression.ConclusionsThe deep learning algorithm provides high auxiliary diagnostic efficiency in patients with AE-IPF and may serve as a useful clinical aid for diagnosis.

show abstract

“…Interestingly, ACP5 levels in the serum derived from control subjects were low, and higher levels of ACP5 were detected in the serum samples from IPF patients ( Figure 1A). Then, we assessed the correlation between the levels of ACP5 and disease severity, which were estimated by the lung's gas diffusing capacity 33 (as measured by the diffusing capacity of the lungs for carbon monoxide, DLCO). Notably, the levels of ACP5 were higher in severe IPF patients whose DLCO was less than 40% of the predicted value than in patients with less severe IPF ( Figure 1B).…”

Section: Ipf Is Characterized By Altered Acp5 Expressionmentioning

confidence: 99%

Tartrate-resistant acid phosphatase 5 serves as a viable target against pulmonary fibrosis by modulating β-catenin signaling

Hu¹,

Yu²,

Wang³

et al. 2020

Preprint

View full text Add to dashboard Cite

Idiopathic pulmonary fibrosis (IPF) is a fatal interstitial lung disease with limited therapeutic options. Tartrate-resistant acid phosphatase 5 (ACP5) performs a variety of functions. However, its role in IPF remains unclear. Here, we demonstrated that the levels of ACP5 were increased in IPF patient samples and mice with bleomycin (BLM)-induced pulmonary fibrosis. In particular, higher levels of ACP5 were noted in the sera of IPF patients with a diffusing capacity of the lungs for carbon monoxide (DLCO) less than 40% of the predicted value. Additionally, Acp5 deficiency protected mice from BLM-induced lung injury and fibrosis and reduced the differentiation and proliferation of fibroblasts. Mechanistic studies revealed that Acp5 was upregulated by TGF-β1 in a TGFβR1/Smad3-dependent manner, after which Acp5 dephosphorylated p-β-catenin at Ser33 and Thr41, inhibiting the degradation of β-catenin and subsequently enhancing β-catenin signaling in the nucleus, which promoted the differentiation and proliferation of fibroblast. Notably, the treatment of mice with BLM-induced fibrosis with Acp5 siRNA-loaded liposomes robustly reversed lung fibrosis. Collectively, these data indicate that Acp5 plays an essential role in the initiation and progression of pulmonary fibrosis; therefore, strategies aimed at silencing Acp5 could be novel therapeutic approaches against pulmonary fibrosis in a clinical setting.

show abstract

Impact of Depression on Patients With Idiopathic Pulmonary Fibrosis

Cited by 30 publications

References 45 publications

Tartrate-resistant acid phosphatase 5 promotes pulmonary fibrosis by modulating β-catenin signaling

Tartrate-resistant acid phosphatase 5 promotes pulmonary fibrosis by modulating β-catenin signaling

Novel 3D-based deep learning for classification of acute exacerbation of idiopathic pulmonary fibrosis using high-resolution CT

Tartrate-resistant acid phosphatase 5 serves as a viable target against pulmonary fibrosis by modulating β-catenin signaling

Contact Info

Product

Resources

About