The extracellular matrix (ECM) is a complex network of proteins and proteoglycans secreted by keratinocytes, fibroblasts and immune cells. The function of the skin ECM has expanded from being a scaffold that provides structural integrity, to a more dynamic entity that is constantly remodeled to maintain tissue homeostasis. The ECM functions as ligands for cell surface receptors such as integrins, dystroglycans, and toll-like receptors (TLRs) and regulate cellular signaling and immune cell dynamics. The ECM also acts as a sink for growth factors and cytokines, providing critical cues during epithelial morphogenesis. Dysregulation in the organization and deposition of ECMs lead to a plethora of pathophysiological conditions that are exacerbated by aberrant ECM-immune cell interactions. In this review, we focus on the interplay between ECM and immune cells in the context of skin diseases and also discuss state of the art therapies that target the key molecular players involved.
Department of Internal Medicine, Division of Diabetes, Endocrinology, and Metabolism, University of Nebraska Medical Center, Omaha, NE, USA; VA Nebraska-Western Iowa Health Care System, Omaha, NE, USA; Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, USA. Electronic address:
The investigation into relaxin (RLN), additional RLN-like proteins, and RLN family peptide receptors (RXFP) has demonstrated their role in modulating the extracellular matrix (ECM), immune cells, specifically macrophages, and angiogenesis, with recent evidence showing an effect on signaling pathways in tumor cells. These findings serve as the basis for our narrative review to collate pertinent studies in this field and provide our perspective on their clinical and investigational significance. In the article, we discuss findings from pertinent studies focusing on evaluating the expression or effect of RLN1, RLN2, or RXFP1 in various cancers.
Hepatocellular carcinoma (HCC) continues to pose a global health concern, necessitating the exploration of innovative therapeutic approaches. In the recent decade, targeting tumor stroma consisting of extracellular matrix (ECM), immune cells, vascular system, hypoxia, and also suppressive mechanisms in HCC has attracted interest in repressing tumor growth and metastasis. Phytochemicals have attained considerable attention because of their manifold biological effects and high capacity for anticancer activities.
Pancreatic cancer is a major health challenge with few effective treatments, largely influenced by its tumor stroma, which consists of various non-cancerous cells and proteins that aid tumor growth and drug resistance.
Targeting the tumor stroma by remodeling it with phytochemicals—natural compounds found in plants—shows promise for enhancing the effects of chemotherapy and immunotherapy by disrupting the communication between tumor cells and their environment.
The review discusses how phytochemicals can modify the tumor stroma and explores their potential in combination with existing cancer treatments, emphasizing their anti-cancer, immunomodulatory, and anti-angiogenic properties.
Pancreatic ductal adenocarcinoma (PDAC) has a poor prognosis due to its fibrotic tumor microenvironment, which inhibits immune cell infiltration, but higher natural killer (NK) cell presence is linked to better survival rates.
Using imaging mass cytometry, researchers found active NK cells in the PDAC tumor microenvironment, interacting with tumor cells while their infiltration was limited by fibrosis.
The study identifies key interactions between NK cells and extracellular matrix components, suggesting that targeting these interactions could enhance NK cell invasion in PDAC, potentially improving treatment outcomes.
Background: Despite the advancements in heart failure(HF) research, the early diagnosis of HF continues to be a challenging issue in clinical practice. This study aims to investigate the genes related to myocardial fibrosis and conduction block, with the goal of developing a diagnostic model for early treatment of HF in patients.
Method: The gene expression profiles of GSE57345, GSE16499, and GSE9128 were obtained from the Gene Expression Omnibus (GEO) database.
