Biomarkers in idiopathic pulmonary fibrosis: Current insight and future direction

Chinese Medical Journal - Pulmonary and Critical Care Medicine, Journal Year: 2024, Volume and Issue: 2(2), P. 72 - 79

Published: June 1, 2024

Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive interstitial lung disease with dismal prognosis. Early diagnosis, accurate prognosis, personalized therapeutic interventions are essential for improving patient outcomes. Biomarkers, as measurable indicators of biological processes or states, hold significant promise in IPF management. In recent years, there has been growing interest identifying validating biomarkers IPF, encompassing various molecular, imaging, clinical approaches. This review provides an in-depth examination the current landscape biomarker research, highlighting their potential applications treatment response. Additionally, challenges future perspectives integration into practice precision medicine discussed.

Language: Английский

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Persisting Shadows: Unraveling the Impact of Long COVID-19 on Respiratory, Cardiovascular, and Nervous Systems

Infectious Disease Reports, Journal Year: 2023, Volume and Issue: 15(6), P. 806 - 830

Published: Dec. 15, 2023

The coronavirus disease 2019 (COVID-19), instigated by the zoonotic Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), rapidly transformed from an outbreak in Wuhan, China, into a widespread global pandemic. A significant post-infection condition, known as 'long- COVID-19' (or simply COVID'), emerges substantial subset of patients, manifesting with constellation over 200 reported symptoms that span multiple organ systems. This also 'post-acute sequelae SARS-CoV-2 infection' (PASC), presents perplexing clinical picture far-reaching implications, often persisting long after acute phase. While initial research focused on immediate pulmonary impact virus, recognition COVID-19 multiorgan disruptor has unveiled gamut protracted and severe health issues. review summarizes primary effects COVID respiratory, cardiovascular, nervous It delves mechanisms underlying these impacts underscores critical need for comprehensive understanding COVID's pathogenesis.

Language: Английский

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Pharmacological approaches to pulmonary fibrosis following COVID-19

Frontiers in Pharmacology, Journal Year: 2023, Volume and Issue: 14

Published: June 15, 2023

In the past few years, COVID-19 became leading cause of morbidity and mortality worldwide. Although World Health Organization has declared an end to as a public health emergency, it can be expected, that emerging new cases at top previous ones will result in increasing number patients with post-COVID-19 sequelae. Despite fact majority recover, severe acute lung tissue injury susceptible individuals progress interstitial pulmonary involvement. Our goal is provide overview various aspects associated Post-COVID-19 fibrosis focus on its potential pharmacological treatment options.

Language: Английский

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Post‐COVID‐19 pulmonary fibrosis: Mechanisms, biomarkers, and therapeutic perspectives

Clinical and Translational Discovery, Journal Year: 2025, Volume and Issue: 5(1)

Published: Feb. 1, 2025

Abstract Post‐COVID‐19 pulmonary fibrosis (post‐CPF) has emerged as a serious complication with profound implications for long‐term respiratory health. This short review explores the multifactorial mechanisms underlying post‐CPF, emphasising role of oxidative stress, epithelial‐to‐mesenchymal transition (EMT), and dysregulated immune responses. Key signalling pathways, such TGF‐β, WNT, Cadherin, are pivotal in progression, offering potential therapeutic targets. Biomarkers, MUC4, KRT5, ATP12A show promise early detection targeting, they share molecular features idiopathic (IPF) fibrotic interstitial lung diseases (f‐ILDs), suggesting opportunities to repurpose antifibrotic therapies. Despite these advancements, significant gaps remain understanding cellular hindering effective management post‐CPF. Addressing challenges through targeted approach is critical improving outcomes survivors severe COVID‐19.

Language: Английский

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Morphopathology of the lesions induced by SARS-CoV-2 infection in the lungs

Romanian Journal of Morphology and Embryology, Journal Year: 2025, Volume and Issue: 65(4), P. 637 - 645

Published: Feb. 13, 2025

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection spread rapidly from China around the world, causing worst pandemic since beginning of 21st century. Although disease named 2019 (COVID-19) has multiple organ symptoms, main pathological lesions occur in lung, failure, pulmonary embolism, secondary bacterial pneumonia and fibrosis. Despite best efforts researchers, pathogenesis SARS-CoV-2-induced cellular tissue damage organs systems is poorly understood. Therefore, our study, we aimed to highlight their extent, which could explain complex symptomatology presented by patients who died with distress (ARDS). The study was performed on a number 36 diagnosed COVID-19 under legally suspicious conditions, requiring autopsy within Romanian Forensic Medicine Institutes. All local inflammatory reaction pneumonic type, exudative proliferative phenomena, intra-alveolar interstitial infiltrates formed lymphocytes, macrophages neutrophilic granulocytes, congested or ruptured blood vessels hemorrhages, thrombosis, proliferation fibroblasts transformed into myofibroblasts presence granulation that remodeled entire lung parenchyma.

Language: Английский

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New evidence for T-cadherin in COVID-19 pathogenesis, endothelial dysfunction, and lung fibrosis

Frontiers in Cell and Developmental Biology, Journal Year: 2025, Volume and Issue: 13

Published: March 5, 2025

The COVID-19 pandemic had an unprecedented impact on all aspects of human activity worldwide, frequently resulting in post-acute sequelae and affecting multiple organ systems. underlying mechanisms driving both acute manifestations are still poorly understood, warranting further investigation for new targets. study represents the first attempt to explore role T-cadherin pathogenesis as well its implications pulmonary fibrosis endothelial dysfunction. First, we revealed a significant decrease expression post-mortem lung samples from patients. This downregulated correlated with elevated levels VE-cadherin reduced β-catenin, suggesting disruption cell-cell contact integrity function. Second, reciprocal relation was confirmed using cultured Ea.hy926 cells. overexpression caused mRNA cells providing additional evidence favor their interplay. Third, employing Cdh13 -/- mice, unveiled protective deficiency against bleomycin-induced fibrosis. Fourth, demonstrated mice lacking have reactive oxygen species production Nox2 angiotensin II-mediated dysfunction model. Our findings provide rationale studies into T-cadherin-mediated these processes.

Language: Английский

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Advances in Therapeutics for Chronic Lung Diseases: From Standard Therapies to Emerging Breakthroughs

Journal of Clinical Medicine, Journal Year: 2025, Volume and Issue: 14(9), P. 3118 - 3118

Published: April 30, 2025

Background: The global health burden of chronic respiratory diseases, such as obstructive pulmonary disease (COPD), asthma, idiopathic fibrosis (IPF), and acute distress syndrome (ARDS) affects billions people is associated with high levels healthcare expenditure. Conventional therapies (bronchodilators corticosteroids) provide symptomatic benefit but take no effect on progression, demonstrating the need to develop new therapies. Emerging treat underlying mechanisms these which relief disease. Methods: This review assesses evolution therapeutic interventions for lung diseases from a series established inhaled combination biologics, gene therapy, even AI-based stratification patients. In addressing issues, we action, evidence efficacy, clinical trial evidence, while discussing access issues affecting implementation ethical in relation their use. Results: highlights recent developments treatment approaches, aimed at cystic mutations, advanced drug delivery pathways more accurate targeting, stem cell-based designed replace damaged tissue. These have potential improve outcomes challenges, including lack access, adequate patient selection, long-term safety, be addressed. Conclusions: New offer tremendous potential, transition laboratory clinic still face numerous barriers regulation, personalized therapy approaches. indicates that future research should strategies reduce distribution, guidelines successfully implement

Language: Английский

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The roles of macrophages and monocytes in COVID-19 Severe Respiratory Syndrome

Cell Insight, Journal Year: 2025, Volume and Issue: unknown, P. 100250 - 100250

Published: May 1, 2025

Language: Английский

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COVID-19: A threat to the respiratory system

International Journal of Immunopathology and Pharmacology, Journal Year: 2024, Volume and Issue: 38

Published: Jan. 1, 2024

The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), causes coronavirus disease-19 (COVID-19) that has emerged on a pandemic level. Coronaviruses are well-known to have negative impact the lungs and cardiovascular system. SARS-CoV-2 induces cytokine storm primarily targets lungs, causing widespread clinical disorders, including COVID-19. Although, positive individuals often show no or mild upper tract symptoms, cases can progress distress (ARDS). Novel CoV-2 infection in 2019 resulted viral pneumonia as well other complications extrapulmonary manifestation. ARDS is also linked higher risk of death. Now, it essential develop our perception long term sequelae for identification COVID-19 survivors who at developing chronic lung fibrosis. This review study was planned provide an overview effects various parts system such airways, pulmonary vascular, parenchymal neuromuscular potential mechanism related fibrosis patients with

Language: Английский

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Molecular Regulation of Transforming Growth Factor-β1-induced Thioredoxin-interacting Protein Ubiquitination and Proteasomal Degradation in Lung Fibroblasts: Implication in Pulmonary Fibrosis

Deleted Journal, Journal Year: 2024, Volume and Issue: 1(1), P. 10002 - 10002

Published: Jan. 1, 2024

Thioredoxin-interacting protein (TXNIP) plays a critical role in regulation of cellular redox reactions and inflammatory responses by interacting with thioredoxin (TRX) or the inflammasome. The TXNIP lung fibrosis molecular its stability have not been well studied. Therefore, here we investigated TGF-β1-mediated signaling fibroblasts. levels were significantly decreased tissues from bleomycin-challenged mice. Overexpression attenuated transforming growth factor-β1 (TGF-β1)-induced phosphorylation Smad2/3 fibronectin expression fibroblasts, suggesting that decrease may contribute to pathogenesis fibrosis. Further, observed TGF-β1 lowered levels, while mRNA unaltered exposure. induced degradation via ubiquitin-proteasome system. A serine residue mutant (TNXIP-S308A) was resistant TGF-β1-induced degradation. Furthermore, downregulation ubiquitin-specific protease-13 (USP13) promoted ubiquitination Mechanistic studies revealed USP13 targeted deubiquitinated TXNIP. results this study lungs apparently contributes pulmonary can target TXNP for deubiquitination regulate stability.

Language: Английский

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