Secuelas inesperadas: cómo la COVID-19 puede afectar tus pulmones a largo plazo DOI Creative Commons

Liliana Faridi Saavedra Salazar,

Juan Armendáriz‐Borunda, Jesús García‐Bañuelos

et al.

Published: April 20, 2024

La pandemia de COVID-19 ha afectado a millones personas en todo el mundo, causando secuelas como la fibrosis pulmonar. Esta condición se desarrolla principalmente pacientes graves durante fase aguda enfermedad, pero también puede aparecer tras recuperación. Es más común con obesidad, tabaquismo, diabetes o que necesitaron ventilación mecánica. Aunque hay muchos casos reportados, faltan estudios para comprender completamente enfermedad y encontrar tratamientos adecuados. atención médica actual centra prevenir desarrollo pulmonar etapas tempranas infección.

Crosstalk between ROS-inflammatory gene expression axis in the progression of lung disorders DOI
Sumel Ashique, Neeraj Mishra, Shubhrajit Mantry

et al.

Naunyn-Schmiedeberg s Archives of Pharmacology, Journal Year: 2024, Volume and Issue: unknown

Published: Aug. 28, 2024

Language: Английский

Citations

8

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

Urvinder Kaur Sardarni,

Siddappa N. Byrareddy

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

Citations

0

Long COVID update: respiratory sequelae and symptoms DOI

Muhammad Mamoon Iqbal,

Ayesha Iqbal, Rachael A. Evans

et al.

Current Opinion in Supportive and Palliative Care, Journal Year: 2025, Volume and Issue: unknown

Published: April 2, 2025

Long COVID affects approximately 6% of the population after SARS-CoV-2 infection commonly involving persistent respiratory symptoms such as breathlessness and cough. This review provides an update on latest evidence regarding post-COVID condition/Long sequelae, focusing symptoms, complications, therapeutic approaches to date. Post-COVID interstitial lung abnormalities are estimated persist in 11% patients hospitalized with acute COVID-19. However, is common adults (non-hospitalized) COVID, suggesting aetiologies beyond pneumonitis. The risk venous thromboembolic disease remains uncertain trial results anti-coagulation awaited. presents complex challenges, careful assessment crucial differentiate from exacerbations pre-existing conditions. Current management includes a symptom-based multidisciplinary approach, ongoing research into effective treatments including immune modulating agents.

Language: Английский

Citations

0

The Nexus of Inflammation-Induced Epithelial-Mesenchymal Transition and Lung Cancer Progression: A Roadmap to Pentacyclic Triterpenoid-Based Therapies DOI Open Access
Kirill V. Odarenko, Marina A. Zenkova, Andrey V. Markov

et al.

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(24), P. 17325 - 17325

Published: Dec. 10, 2023

Lung cancer is the leading cause of cancer-related death worldwide. Its high mortality partly due to chronic inflammation that accompanies disease and stimulates progression. In this review, we analyzed recent studies highlighted role epithelial-mesenchymal transition (EMT) as a link between lung cancer. inflammatory tumor microenvironment (iTME), fibroblasts, macrophages, granulocytes, lymphocytes produce mediators, some which can induce EMT. This leads increased invasiveness cells self-renewal stem (CSCs), are associated with metastasis recurrence, respectively. Based on published data, propose inflammation-induced EMT may be potential therapeutic target for treatment prospect partially realized in development inhibitors based pentacyclic triterpenoids (PTs), described second part our study. PTs reduce metastatic stemness cells, making promising candidates therapy. We emphasize diversity molecular mechanisms underlying far exceeds those have been implicated drug development. Therefore, analysis information relationship iTME great interest provide ideas novel approaches

Language: Английский

Citations

9

Immune and non-immune mediators in the fibrosis pathogenesis of salivary gland in Sjögren’s syndrome DOI Creative Commons

Danbao Ma,

Yun Feng,

Xiang Lin

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: Oct. 14, 2024

Sjögren’s syndrome (SS) or disease (SjD) is a systemic autoimmune clinically manifested as sicca symptoms. This primarily impacts the functionality of exocrine glands, specifically lacrimal and salivary glands (SG). SG fibrosis, an irreversible morphological change, severe consequence that occurs in later stages due to sustained inflammation. However, mechanism underlying fibrosis SS remains under-investigated. Glandular may arise from chronic sialadenitis, which interactions between infiltrating lymphocytes epithelial cells potentially contributes fibrotic pathogenesis. Thus, both immune non-immune are closely involved this process, while their interplays not fully understood. The molecular tissue partly associated with imbalance responses, transforming growth factor-beta (TGF-β)-dependent epithelial-mesenchymal transition (EMT) extracellular matrix remodeling recently investigated. In addition, viral infection has been implicated pathogenesis SS. Viral-specific innate response could exacerbate progression, resulting overt inflammation SG. Notably, post-COVID patients exhibit typical symptoms inflammatory positively correlated damage. review, we discuss risk factors summarize evidence understand mechanisms upon progression

Language: Английский

Citations

3

The role of epithelial-mesenchymal transition in pulmonary fibrosis: lessons from idiopathic pulmonary fibrosis and COVID-19 DOI Creative Commons

Reyhaneh Niayesh‐Mehr,

Mojtaba Kalantar, Giulio Bontempi

et al.

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

Published: Nov. 13, 2024

Despite the tremendous advancements in knowledge of pathophysiology and clinical aspects SARS-CoV-2 infection, still many issues remain unanswered, especially long-term effects. Mounting evidence suggests that pulmonary fibrosis (PF) is one most severe complications associated with COVID-19. Therefore, understanding molecular mechanisms behind its development helpful to develop successful therapeutic strategies. Epithelial mesenchymal transition (EMT) cell specific variants endothelial (EndMT) mesothelial (MMT) are physio-pathologic cellular reprogramming processes induced by several infectious, inflammatory biomechanical stimuli. Cells undergoing EMT acquire invasive, profibrogenic proinflammatory activities secreting extracellular mediators. Their activity has been implicated pathogenesis PF a variety lung disorders, including idiopathic (IPF) Aim this article provide an updated survey mechanisms, emphasis on EMT-related processes, genesis IFP

Language: Английский

Citations

3

Perspectives on Post-COVID-19 Pulmonary Fibrosis Treatment DOI Open Access
Elena Cojocaru,

Tudor Cojocaru,

Giulia Mihaela Pînzariu

et al.

Journal of Personalized Medicine, Journal Year: 2023, Volume and Issue: 14(1), P. 51 - 51

Published: Dec. 29, 2023

Pulmonary fibrosis, a critical outcome of chronic inflammatory diseases, has gained prominence in the context post-coronavirus (post-COVID-19) complications. This review delves into multifaceted landscape post-COVID-19 pulmonary elucidating intricate molecular mechanisms underlying its pathogenesis and highlighting promising therapeutic avenues. Examining aftermath severe acute respiratory syndrome-2 (SARS-CoV-2) infection, reveals key signaling pathways implicated fibrotic cascade. Drawing parallels with previous coronavirus outbreaks enhances our understanding distinctive features fibrosis. Antifibrotic drugs, like pirfenidone nintedanib, take center stage; their action potential applications cases are thoroughly explored. Beyond established treatments, this investigates emerging modalities, including anti-interleukin agents, immunosuppressants, experimental compounds, buloxybutide, saracatinib, sirolimus, resveratrol. Emphasizing importance early intervention, highlights dynamic nature fibrosis research. In conclusion, synthesis current knowledge offers foundation for advancing approaches to prevention treatment these consequential sequelae COVID-19.

Language: Английский

Citations

4

Luteolin alleviates airway remodeling in asthma by inhibiting the epithelial-mesenchymal transition via β-catenin regulation DOI
Jingyu Quan, Dan Xie, Zihong Li

et al.

Phytomedicine, Journal Year: 2024, Volume and Issue: 135, P. 156090 - 156090

Published: Oct. 3, 2024

Language: Английский

Citations

1

Unmetabolized folic acid and organ fibrosis: Are they nefarious partners? DOI
Larry B. Goldstein,

Luca Mascitelli

Medical Hypotheses, Journal Year: 2024, Volume and Issue: 186, P. 111323 - 111323

Published: March 15, 2024

Language: Английский

Citations

1

1-L Transcription of SARS-CoV-2 Spike Protein S1 Subunit DOI Open Access
Jozef Nahálka

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(8), P. 4440 - 4440

Published: April 18, 2024

The COVID-19 pandemic prompted rapid research on SARS-CoV-2 pathogenicity. Consequently, new data can be used to advance the molecular understanding of infection. present bioinformatics study discusses "spikeopathy" at level and focuses possible post-transcriptional regulation spike protein S1 subunit in host cell/tissue. A theoretical protein-RNA recognition code was check compatibility with mRNAs human transcriptome (1-L transcription). principle for this method is elucidated defined RNA binding GEMIN5 (gem nuclear organelle-associated 5) RNU2-1 (U2 spliceosomal RNA). Using described here, it shown that 45% genes/proteins identified by 1-L transcription are directly linked COVID-19, 39% indirectly 16% cannot currently associated COVID-19. stroke, diabetes, cardiac injury.

Language: Английский

Citations

1