TIMP-1 and its potential diagnostic and prognostic value in pulmonary diseases

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Abstract

Tissue inhibitors of metalloproteases (TIMPs) have caught the attention of many scientists due to their role in various physiological and pathological processes. TIMP-1, 2, 3, and 4 are known members of the TIMPs family. TIMPs exert their biological effects by, but are not limited to, inhibiting the activity of metalloproteases (MMPs). The balance between MMPs and TIMPs is critical for maintaining homeostasis of the extracellular matrix (ECM), while the imbalance between MMPs and TIMPs can lead to pathological changes, such as cancer. In this review, we summarized the current knowledge of TIMP-1 in several pulmonary diseases namely, acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), pneumonia, asthma, chronic obstructive pulmonary disease (COPD), cystic fibrosis, and pulmonary fibrosis. Considering the potential of TIMP-1 serving as a non-invasive diagnostic and/or prognostic biomarker, we also reviewed the circulating TIMP-1 levels in translational and clinical studies.

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Acute respiratory distress syndrome

Michael Matthay, Rachel L. Zemans, Guy Zimmerman … (2019)

The acute respiratory distress syndrome (ARDS) is a common cause of respiratory failure in critically ill patients and is defined by the acute onset of noncardiogenic pulmonary oedema, hypoxaemia and the need for mechanical ventilation. ARDS occurs most often in the setting of pneumonia, sepsis, aspiration of gastric contents or severe trauma and is present in ~10% of all patients in intensive care units worldwide. Despite some improvements, mortality remains high at 30–40% in most studies. Pathological specimens from patients with ARDS frequently reveal diffuse alveolar damage, and laboratory studies have demonstrated both alveolar epithelial and lung endothelial injury, resulting in accumulation of protein-rich inflammatory oedematous fluid in the alveolar space. Diagnosis is based on consensus syndromic criteria, with modifications for under-resourced settings and in paediatric patients. Treatment focuses on lung-protective ventilation; no specific pharmacotherapies have been identified. Long-term outcomes of patients with ARDS are increasingly recognized as important research targets, as many patients survive ARDS only to have ongoing functional and/or psychological sequelae. Future directions include efforts to facilitate earlier recognition of ARDS, identifying responsive subsets of patients and ongoing efforts to understand fundamental mechanisms of lung injury to design specific treatments.

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Idiopathic pulmonary fibrosis.

Luca Richeldi, Harold Collard, Mark G. Jones (2017)

Idiopathic pulmonary fibrosis is a prototype of chronic, progressive, and fibrotic lung disease. Healthy tissue is replaced by altered extracellular matrix and alveolar architecture is destroyed, which leads to decreased lung compliance, disrupted gas exchange, and ultimately respiratory failure and death. In less than a decade, understanding of the pathogenesis and management of this disease has been transformed, and two disease-modifying therapies have been approved, worldwide. In this Seminar, we summarise the presentation, pathophysiology, diagnosis, and treatment options available for patients with idiopathic pulmonary fibrosis. This disease has improved understanding of the mechanisms of lung fibrosis, and offers hope that similar approaches will transform the management of patients with other progressive fibrotic lung diseases.

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New insights into TGF-β/Smad signaling in tissue fibrosis

Ying-Yong Zhao, He-He Hu, Dan-Qian Chen … (2018)

Transforming growth factor-β1 (TGF-β1) is considered as a crucial mediator in tissue fibrosis and causes tissue scarring largely by activating its downstream small mother against decapentaplegic (Smad) signaling. Different TGF-β signalings play different roles in fibrogenesis. TGF-β1 directly activates Smad signaling which triggers pro-fibrotic gene overexpression. Excessive studies have demonstrated that dysregulation of TGF-β1/Smad pathway was an important pathogenic mechanism in tissue fibrosis. Smad2 and Smad3 are the two major downstream regulator that promote TGF-β1-mediated tissue fibrosis, while Smad7 serves as a negative feedback regulator of TGF-β1/Smad pathway thereby protects against TGF-β1-mediated fibrosis. This review presents an overview of the molecular mechanisms of TGF-β/Smad signaling pathway in renal, hepatic, pulmonary and cardiac fibrosis, followed by an in-depth discussion of their molecular mechanisms of intervention effects both in vitro and in vivo. The role of TGF-β/Smad signaling pathway in tumor or cancer is also discussed. Additionally, the current advances also highlight targeting TGF-β/Smad signaling pathway for the prevention of tissue fibrosis. The review reveals comprehensive pathophysiological mechanisms of tissue fibrosis. Particular challenges are presented and placed within the context of future applications against tissue fibrosis.

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Journal

Journal ID (nlm-journal-id): 9918627881206676

Journal ID (pubmed-jr-id): 52660

Journal ID (nlm-ta): Chin Med J Pulm Crit Care Med

Journal ID (iso-abbrev): Chin Med J Pulm Crit Care Med

Title: Chinese medical journal pulmonary and critical care medicine

ISSN (Electronic): 2772-5588

Publication date Nihms-submitted: 4 August 2023

Publication date (Print): June 2023

Publication date (Electronic): 19 June 2023

Publication date PMC-release: 09 February 2024

Volume: 1

Issue: 2

Pages: 67-76

Affiliations

[1 ]Clinical and Experimental Therapeutics, Department of Clinical and Administrative Pharmacy, College of Pharmacy, University of Georgia and Charlie Norwood VA Medical Center, Augusta, GA 30912, USA

[2 ]Department of Clinical Pharmacy, College of Pharmacy, University of Hail, Hail 55473, Saudi Arabia

[3 ]Department of Emergency Medicine, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA

[4 ]Department of Medicine, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA

Author notes

[* ]Correspondence to: Clinical and Experimental Therapeutics, Department of Clinical and Administrative Pharmacy, College of Pharmacy, University of Georgia and Charlie Norwood VA Medical Center, Augusta, GA 30912, USA. duozhang@ 123456uga.edu (D. Zhang)

[** ]Correspondence to: Department of Medicine, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA. xiaoyunwang@ 123456uga.edu (X. Wang)

Article

Manuscript ID: NIHMS1914669

DOI: 10.1016/j.pccm.2023.05.002

PMC ID: 10857872

PubMed ID: 38343891

SO-VID: a6b99956-e187-4c29-a28f-f2e857f63f59

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This is an open access article under the CC BY-NC-ND license ( http://creativecommons.org/licenses/by-nc-nd/4.0/)

TIMP-1 and its potential diagnostic and prognostic value in pulmonary diseases

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Abstract

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Biomarkers for Inflammatory Lung Disease

Most cited references 159

Acute respiratory distress syndrome

Idiopathic pulmonary fibrosis.

New insights into TGF-β/Smad signaling in tissue fibrosis

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