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The Role of Extracellular Matrix Proteins in Pathogenesis: 2nd Edition
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The Role of Extracellular Matrix Proteins in Pathogenesis: 2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 October 2025 | Viewed by 2018

Special Issue Editor

Dr. Davide Raineri

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Guest Editor
Department of Health Sciences, University of Piemonte Orientale, 28100 Novara, Italy
Interests: osteopontin; cancers; autoimmune diseases; inflammation; chronic diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Extracellular matrix (ECM) proteins play a crucial role in the pathogenesis of various diseases by contributing to tissue remodeling, cell signaling, and immune response modulation. The ECM is a complex network of proteins and other molecules that provides structural support and regulates cell behavior in tissues. In the context of disease pathogenesis, ECM proteins play crucial roles in various pathological processes. One of the key functions of ECM proteins is to maintain tissue integrity and architecture. Disruption or dysregulation of ECM proteins can lead to tissue remodeling, fibrosis, and impaired organ function. For example, in diseases like pulmonary fibrosis or liver cirrhosis, excessive deposition of ECM proteins, particularly collagens, disrupts the normal tissue architecture, resulting in organ dysfunction. Moreover, ECM proteins serve as signaling molecules and interact with cell surface receptors to modulate cellular behavior. A class of ECM receptors called integrins is essential for cell adhesion, migration, and proliferation. Dysregulation of ECM–integrin interactions can contribute to the progression of cancer by promoting tumor cell invasion and metastasis. ECM proteins are also involved in inflammatory disorders like autoimmune disease. In conditions such as rheumatoid arthritis, inflammatory cells release enzymes called matrix metalloproteinases (MMPs), which degrade ECM proteins, leading to joint destruction and tissue damage. In contrast, excessive ECM protein deposition in chronic inflammatory diseases like atherosclerosis can cause plaque development and arterial stiffness. In summary, ECM proteins play multifaceted roles in disease pathogenesis. Their dysregulation disrupts tissue homeostasis, promotes inflammation, facilitates tumor progression, and contributes to fibrosis and cardiovascular disorders. Understanding the complex interplay between ECM proteins and disease processes is crucial for developing therapeutic strategies that target the ECM to alleviate disease progression and improve patient outcomes.

This Special Issue aims to bring together research articles and reviews that help to understand those still unknown molecular mechanisms of ECM proteins in the pathogenesis of diseases.

Dr. Davide Raineri
Guest Editor

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Keywords

  • extracellular matrix proteins
  • autoimmune disease
  • cancer
  • cardiovascular diseases
  • inflammation
  • chronic diseases
  • human diseases

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Published Papers (5 papers)

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Research

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15 pages, 3528 KiB  
Article
Acetylcholine Sustains LNCaP Prostate Cancer Cell Migration, Invasion and Proliferation Through Glyoxalase 1/MG-H1 Axis with the Involvement of Osteopontin
by Dominga Manfredelli, Tatiana Armeni, Lidia de Bari, Andrea Scirè, Vincenzo Nicola Talesa, Cinzia Antognelli and Marilena Pariano
Int. J. Mol. Sci. 2025, 26(9), 4107; https://doi.org/10.3390/ijms26094107 - 25 Apr 2025
Viewed by 110
Abstract
The neurotransmitter acetylcholine (ACh) plays a pro-carcinogenic role in various cancer types, including prostate cancer (PCa). The existing body of knowledge concerning the mechanisms that underpin the protumoral role of ACh in PCa is limited. Glyoxalase 1 (Glo1) is a metabolic enzyme that [...] Read more.
The neurotransmitter acetylcholine (ACh) plays a pro-carcinogenic role in various cancer types, including prostate cancer (PCa). The existing body of knowledge concerning the mechanisms that underpin the protumoral role of ACh in PCa is limited. Glyoxalase 1 (Glo1) is a metabolic enzyme that removes methylglyoxal (MG), an endogenous post-translational modification agent, generating 5-hydro-5-methylimidazolone (MG-H1). The Glo1/MG-H1 axis is involved in PCa tumorigenesis and progression. By using LNCaP and PC3 PCa cells, representing extensively studied cell models of poorly aggressive and bone metastasis-derived PCa, respectively, we found that ACh specifically sustains LNCaP cell migration, invasion and proliferation through Glo1-dependent MG-H1 accumulation with the involvement of osteopontin (OPN), thus providing a novel mechanism underlying ACh’s protumoral role in PCa cells. The findings of this study unveil a hitherto unidentified mechanism implicated in the progression of PCa, which is initiated by ACh and involves both the Glo1/MG-H1 axis and OPN. This discovery provides the basis for new avenues of in vivo investigation into the physiological relevance of the roles of the ACh-driven Glo1/MG-H1 axis and OPN in PCa progression and for further research aimed at exploring new ways of managing PCa progression, with the aim of preventing the disease from becoming incurable. Full article
(This article belongs to the Special Issue The Role of Extracellular Matrix Proteins in Pathogenesis: 2nd Edition)
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12 pages, 3397 KiB  
Article
Chymase Inhibition Attenuates Kidney Fibrosis in a Chronic Mouse Model of Renal Ischemia–Reperfusion Injury
by Sakura Kure, Hiroe Toba, Denan Jin, Akira Mima and Shinji Takai
Int. J. Mol. Sci. 2025, 26(8), 3913; https://doi.org/10.3390/ijms26083913 - 21 Apr 2025
Viewed by 165
Abstract
Although various factors contribute to the transition from acute kidney injury (AKI) to chronic kidney disease (CKD), no clinically effective pharmacological treatment has been established. We investigated whether chymase inhibition is effective in preventing renal fibrosis, a key process in the transition from [...] Read more.
Although various factors contribute to the transition from acute kidney injury (AKI) to chronic kidney disease (CKD), no clinically effective pharmacological treatment has been established. We investigated whether chymase inhibition is effective in preventing renal fibrosis, a key process in the transition from AKI to CKD. Male BALB/c mice were subjected to unilateral ischemia-reperfusion (I/R) injury, and TY-51469, a chymase-specific inhibitor, was administered intraperitoneally at a dose of 10 mg/kg/day for 6 weeks. The 45 min ischemic period followed by 6 weeks of reperfusion resulted in severe renal atrophy. Renal fibrosis was particularly pronounced in the transition region between the cortex and medulla in placebo-treated mice. The expression of mouse mast cell protease 4 (MMCP-4, a mouse chymase) mRNA, the number of chymase-positive mast cells, and fibrosis-related factors, such as transforming growth factor (TGF)-β1 and collagen I, were all significantly increased in I/R-injured kidneys. However, treatment with TY-51469 significantly suppressed fibrosis formation, along with the inhibition of renal chymase and TGF-β1 expression. These findings suggest that chymase inhibition may be a potential therapeutic strategy for preventing the transition from AKI to CKD by reducing fibrosis. Full article
(This article belongs to the Special Issue The Role of Extracellular Matrix Proteins in Pathogenesis: 2nd Edition)
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Review

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19 pages, 2497 KiB  
Review
Non-Integrin Laminin Receptors: Shedding New Light and Clarity on Their Involvement in Human Diseases
by Filomena Napolitano, Maria Fabozzi and Nunzia Montuori
Int. J. Mol. Sci. 2025, 26(8), 3546; https://doi.org/10.3390/ijms26083546 - 10 Apr 2025
Viewed by 239
Abstract
The extracellular matrix (ECM) is a dynamic network of macromolecules that provides structural support for cells and orchestrates cell signaling, functions, and morphology. The basement membrane constitutes a peculiar sheet-like type of ECM located between epithelial tissues and underlying connective tissues. The major [...] Read more.
The extracellular matrix (ECM) is a dynamic network of macromolecules that provides structural support for cells and orchestrates cell signaling, functions, and morphology. The basement membrane constitutes a peculiar sheet-like type of ECM located between epithelial tissues and underlying connective tissues. The major constituent of the basement membrane is laminin, which exerts a remarkable repertoire of biological functions such as cell differentiation, migration, adhesion, and wound healing. Laminin performs its functions by interacting with two main classes of receptors, the integrin and the non-integrin laminin receptors, creating a complex network essential for tissue integrity and regeneration. Dysfunctional actions of laminin are the cause of diverse human diseases, including cancer, infectious, and neurodegenerative diseases. This topic has attracted researchers for some time, but the diversity of cell-surface receptors, through which laminin signaling occurs, makes the role of laminin controversial. Moreover, different laminin isoforms were identified, and each specific tissue basement membrane differs from the others in their laminin composition. This review focuses on the structural and molecular basis and pathophysiological relevance of specific interactions between laminins and non-integrin receptors in development, health, and disease. Full article
(This article belongs to the Special Issue The Role of Extracellular Matrix Proteins in Pathogenesis: 2nd Edition)
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27 pages, 1309 KiB  
Review
Cathepsin K Inhibitors as Potential Drugs for the Treatment of Osteoarthritis
by Leyre Brizuela, Rene Buchet, Carole Bougault and Saida Mebarek
Int. J. Mol. Sci. 2025, 26(7), 2896; https://doi.org/10.3390/ijms26072896 - 22 Mar 2025
Viewed by 343
Abstract
Links between cathepsin K and the pathophysiology of osteoarthritis (OA) can be established, not least because of the overabundance of cathepsin K in the serum of OA patients and the upregulation of cathepsin K in degraded cartilage in animal models of OA. Chondrocytes, [...] Read more.
Links between cathepsin K and the pathophysiology of osteoarthritis (OA) can be established, not least because of the overabundance of cathepsin K in the serum of OA patients and the upregulation of cathepsin K in degraded cartilage in animal models of OA. Chondrocytes, chondroclasts, or osteoclasts contribute to the accumulated cathepsin K at the diseased osteochondral junction. After a general presentation of OA and cartilage physiology, as well as its degradation processes, we describe the function of cathepsin K and its effect on cartilage degradation via type II collagen cleavage. An overview of the most promising cathepsin K inhibitors is then presented, together with their in vitro effects. Although intensive research on cathepsin K inhibitors initially focused on bone resorption, there is growing interest in the potential of these drugs to prevent cartilage degradation. In this review, we summarize the pre-clinical and clinical trials that support the use of cathepsin K inhibitors in the treatment of OA. To date, no molecules of this type are commercially available, although a few have undergone clinical trials, but we believe that the development of cathepsin K inhibitors could broaden the therapeutic arsenal for the treatment of OA. Full article
(This article belongs to the Special Issue The Role of Extracellular Matrix Proteins in Pathogenesis: 2nd Edition)
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21 pages, 3247 KiB  
Review
Matrikines of Sea Cucumbers: Structure, Biological Activity and Mechanisms of Action
by Aleksandr Popov, Emma Kozlovskaya, Tatyana Rutckova, Olga Styshova, Vyacheslav Makhankov, Aleksey Vakhrushev, Dmitry Hushpulian, Irina Gazaryan, Oksana Son and Ludmila Tekutyeva
Int. J. Mol. Sci. 2024, 25(22), 12068; https://doi.org/10.3390/ijms252212068 - 10 Nov 2024
Cited by 1 | Viewed by 1071
Abstract
Matrikines (MKs), the products of enzymatic fragmentation of various extracellular matrix (ECM) proteins, regulate cellular activity by interacting with specific receptors. MKs affect cell growth, proliferation, and migration, can induce apoptosis and autophagy, and are also effectively used in biomedicine and functional nutrition. [...] Read more.
Matrikines (MKs), the products of enzymatic fragmentation of various extracellular matrix (ECM) proteins, regulate cellular activity by interacting with specific receptors. MKs affect cell growth, proliferation, and migration, can induce apoptosis and autophagy, and are also effectively used in biomedicine and functional nutrition. Recently, there has been great interest in the structural features and biological activity of MKs from various sources. This review summarized and analyzed the results of modern research on MKs from sea cucumbers, primarily from trepang (MKT). Particular attention is paid to the analysis of the existing knowledge on the antioxidant, anti-inflammatory and adaptogenic activities of these MKs and the possible mechanisms of their protective action. Full article
(This article belongs to the Special Issue The Role of Extracellular Matrix Proteins in Pathogenesis: 2nd Edition)
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