Lung regeneration and lung bioengineering DOI

Edmond Cohen

Current Opinion in Anaesthesiology, Journal Year: 2024, Volume and Issue: unknown

Published: Nov. 28, 2024

Purpose of review Chronic obstructive pulmonary disease affects more than 65 million people worldwide. Lung transplantation is the only definitive treatment. However, donor availability limited in meeting demand. Recent findings regeneration a new therapeutic strategy that uses patient's stem cells to replace dysfunctional tissue and restore functional lung rather alleviate symptoms. Organoids are promising target for human regeneration. The AEP isolated from growth. 3D organ-like structures conserve alveolar progenitor's capacity proliferate differentiate into various epithelial cell types. Bioengineered organs, cells, allow customized biocompatible organs-on-demand without need immunosuppressive therapy. concept involves creation form scaffold, be populated by desired transplanted patient, allowing function as closely native organ possible. Summary lung's ability regenerate extensively after injury suggests this capability could promoted diseases which loss occurs. bioengineering offers potential drastically extend life expectancy patients with end-stage disease. If reengineering were successful, it would revolutionize world transplantation.

Language: Английский

Endothelial cell dynamics in sepsis-induced acute lung injury and acute respiratory distress syndrome: pathogenesis and therapeutic implications DOI Creative Commons

Xinyu Qiao,

Junhao Yin,

Zhihuan Zheng

et al.

Cell Communication and Signaling, Journal Year: 2024, Volume and Issue: 22(1)

Published: April 25, 2024

Abstract Sepsis, a prevalent critical condition in clinics, continues to be the leading cause of death from infections and global healthcare issue. Among organs susceptible harmful effects sepsis, lungs are notably most frequently affected. Consequently, patients with sepsis predisposed developing acute lung injury (ALI), severe cases, respiratory distress syndrome (ARDS). Nevertheless, precise mechanisms associated onset ALI/ARDS remain elusive. In recent years, there has been growing emphasis on role endothelial cells (ECs), cell type integral barrier function, their interactions various stromal sepsis-induced ALI/ARDS. this comprehensive review, we summarize involvement intricate interplay immune cells, including pulmonary epithelial fibroblasts, pathogenesis ALI/ARDS, particular placed discussing several pivotal pathways implicated process. Furthermore, discuss potential therapeutic interventions for modulating functions relevant present strategy managing

Language: Английский

Citations

29
Lung regeneration: diverse cell types and the therapeutic potential DOI Creative Commons
Yutian Chen, Zhen Li, Gaili Ji

et al.

MedComm, Journal Year: 2024, Volume and Issue: 5(2)

Published: Feb. 1, 2024

Abstract Lung tissue has a certain regenerative ability and triggers repair procedures after injury. Under controllable conditions, lung can restore normal structure function. Disruptions in this process lead to respiratory system failure even death, causing substantial medical burden. The main types of diseases are chronic obstructive pulmonary disease (COPD), idiopathic fibrosis (IPF), acute distress syndrome (ARDS). Multiple cells, such as epithelial endothelial fibroblasts, immune involved regulating the Although mechanism that regulates not been fully elucidated, clinical trials targeting different cells signaling pathways have achieved some therapeutic effects diseases. In review, we provide an overview cell type regeneration repair, research models, summarize molecular mechanisms regulation fibrosis. Moreover, discuss current stem therapy pharmacological strategies for COPD, IPF, ARDS treatment. This review provides reference further on cellular regeneration, drug development, trials.

Language: Английский

Citations

11
Biomechanical Properties and Cellular Responses in Pulmonary Fibrosis DOI Creative Commons
Andong He, Lizhe He,

T.‐L. Chen

et al.

Bioengineering, Journal Year: 2024, Volume and Issue: 11(8), P. 747 - 747

Published: July 24, 2024

Pulmonary fibrosis is a fatal lung disease affecting approximately 5 million people worldwide, with 5-year survival rate of less than 50%. Currently, the only available treatments are palliative care and transplantation, as there no curative drug for this condition. The involves excessive synthesis extracellular matrix (ECM) due to alveolar epithelial cell damage, leading scarring stiffening tissue ultimately causing respiratory failure. Although multiple factors contribute disease, exact causes remain unclear. mechanical properties tissue, including elasticity, viscoelasticity, surface tension, not affected by but also its progression. This paper reviews alteration in these pulmonary progresses how cells lung, cells, fibroblasts, macrophages, respond changes, contributing exacerbation. Furthermore, it highlights importance developing advanced vitro models, based on hydrogels 3D bioprinting, which can accurately replicate structural fibrotic lungs conducive studying effects stimuli cellular responses. review aims summarize current understanding interaction between progression alterations properties, could aid development novel therapeutic strategies disease.

Language: Английский

Citations

4
Analysis of Stratifin Expression and Proteome Variation in a Rat Model of Acute Lung Injury DOI Creative Commons
Ayaka Yoshida, Yoshiaki Hashimoto,

Hirotoshi Akane

et al.

Journal of Proteome Research, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 28, 2025

Diffuse alveolar damage (DAD) is a pathological hallmark of severe interstitial lung diseases, such as acute respiratory distress syndrome (ARDS), and linked to poor prognosis. Previously, we identified 14–3–3σ/stratifin (SFN) serum biomarker candidate for diagnosing DAD. To clarify the time-dependent relationship between SFN expression DAD, here investigated molecular changes in serum, bronchoalveolar lavage fluid (BALF), tissue an oleic acid (OA)-induced ARDS rat model. Acute edema was observed after OA administration, followed by epithelial cell proliferation increased BALF levels. Proteomic analysis extracts revealed that proteins related "inflammatory response" "HIF-1 signaling," including plasminogen activator inhibitor-1, were markedly 3 h injury, gradual decrease. Conversely, associated with "cell cycle" "p53 pathway," SFN, showed persistent increase starting at peaking 48 h. Western blotting immunohistochemistry confirmed expressed part proliferated type-II cells, accompanied p53 activation, important event differentiation into type-I cells. may be closely remodeling during repair process injury.

Language: Английский

Citations

0
Protocatechuic Acid Alleviates Inflammation and Oxidative Stress in Acute Respiratory Distress Syndrome by Promoting Unconventional Prefoldin RPB5 Interactor 1‐Mediated Mitophagy DOI Open Access
Xianyong Li,

Quankuan Gu,

Jiaxi Xu

et al.

Chemical Biology & Drug Design, Journal Year: 2025, Volume and Issue: 105(3)

Published: March 1, 2025

ABSTRACT Protocatechuic acid (PCA) is a type of polyphenol with diverse biological activities, including antioxidant and anti‐inflammatory properties. This study aimed to explore the function PCA in acute respiratory distress syndrome (ARDS) delve into its functional mechanism. Lipopolysaccharides were applied stimulate human pulmonary microvascular endothelial cells (HPMECs) or C57BL/6 mice generate ARDS models vitro vivo. treatment (300 μM for 20 30 mg/kg mice) reduced proinflammatory cytokine production oxidative stress HPMECs mouse models, it cell apoptosis while alleviating alveolar septum thickening. Chromobox 4 (CBX4) was identified as target protein PCA, found activate transcription unconventional prefoldin RPB5 interactor 1 (URI1) by recruiting histone acetyltransferase general control nondepressible 5 (GCN5) promoter region. CBX4 URI1 levels LPS but restored PCA. Knockdown either negated ameliorating effects on LPS‐induced inflammation diminished promoting roles mitochondrial biogenesis mitophagy. suggests that holds promise CBX4/URI1‐mediated

Language: Английский

Citations

0
Deciphering the interplay: circulating cell-free DNA, signaling pathways, and disease progression in idiopathic pulmonary fibrosis DOI

Yeva Meshkovska,

Barchinai Dzhuraeva,

Chandraiah Godugu

et al.

3 Biotech, Journal Year: 2025, Volume and Issue: 15(4)

Published: March 29, 2025

Language: Английский

Citations

0
Cytological changes in radiation-induced lung injury DOI
Yun Wang, Jianghong Zhang, Chunlin Shao

et al.

Life Sciences, Journal Year: 2024, Volume and Issue: unknown, P. 123188 - 123188

Published: Oct. 1, 2024

Language: Английский

Citations

2
Protein interactome analysis of ATP1B1 in alveolar epithelial cells using Co-Immunoprecipitation mass spectrometry and parallel reaction monitoring assay DOI Creative Commons

Yu Zheng,

Weiting Peng,

Xu-Peng Wen

et al.

Heliyon, Journal Year: 2024, Volume and Issue: 10(11), P. e32579 - e32579

Published: June 1, 2024

Language: Английский

Citations

1
Inflammatory and Immune Mechanisms in COPD: Current Status and Therapeutic Prospects DOI Creative Commons

Yanan Qi,

Yuanyuan Yan,

Da-Wei Tang

et al.

Journal of Inflammation Research, Journal Year: 2024, Volume and Issue: Volume 17, P. 6603 - 6618

Published: Sept. 1, 2024

Chronic obstructive pulmonary disease (COPD) currently ranks among the top three causes of mortality worldwide, presenting as a prevalent and complex respiratory ailment. Ongoing research has underscored pivotal role immune function in onset progression COPD. The response COPD patients exhibits abnormalities, characterized by diminished anti-infection capacity due to senescence, heightened activation neutrophils macrophages, T cell infiltration, aberrant B activity, collectively contributing airway inflammation lung injury

Language: Английский

Citations

0
Preliminary proteomic analysis of mouse lung tissue treated with cyclophosphamide and Venetin-1 DOI Creative Commons
Paulina Czaplewska, Marc Müller, Natalia Musiał

et al.

Scientific Reports, Journal Year: 2024, Volume and Issue: 14(1)

Published: Oct. 23, 2024

Cyclophosphamide (CPAm) is a widely used chemotherapeutic agent that exhibits potent anti-cancer properties but often associated with debilitating side effects. Despite its efficacy, the management of CPAm-induced toxicities remains significant clinical challenge. There has been growing interest in exploring complementary and alternative therapies to mitigate these adverse effects recent years, this may be chance for earthworm-derived preparation, Venetin-1. Its rich composition bioactive compounds demonstrated promising pharmacological properties, including anti-inflammatory, antioxidant, immunomodulatory These suggest potential counteract various systemic induced by CPAm. We conducted comprehensive study investigate effect Venetin-1 on cyclophosphamide-induced toxicity. Mice were administered CPAm four days, followed application earthworm preparation two doses (50 mg/kg 100 b.w). Importantly, did not cause any all mice, ensuring safety intervention. then determined global changes proteome using proteomics quantitative SWATH-MS analysis, which robust reliable method. This allowed us identify up- downregulated proteins each studied group, providing valuable insights into mechanism action As shown results, had mouse lung tissue. It was possible determine 400 proteins, analysis after administration showed change proteomic profile from upregulated down-regulated. The stimulating concerning complement system also confirmed separate validation experiment. shows promise reducing harmful cyclophosphamide encourages tissue regeneration, reduces inflammation, supports autophagy, boosts immune system. However, more research needed thoroughly elucidate describe benefits

Language: Английский

Citations

0