Role of the lysyl oxidase family in organ development (Review)

Abstract

Lysyl oxidase proteins (LOXs) are amine oxidases, which are mainly located in smooth muscle cells and fibroblasts and serve an important role in the formation of the extracellular matrix (ECM) in a copper-dependent manner. Owing to the ability of LOX proteins to modulate crosslinking between collagens and to promote the deposition of other fibers, they serve crucially in organogenesis and the subsequent organ development, as well as disease initiation and progression. In addition, ECM formation significantly influences organ morphological formation in both cancer-and non-tumor-related diseases, in addition to cellular epigenetic transformation and migration, under the influence of LOXs. A number of different signaling pathways regulate the LOXs expression and their enzymatic activation. The tissue remodeling and transformation process shares some resemblance between oncogenesis and embryogenesis. Additionally the roles that LOXs serve appeared to be stressed during oncogenesis and tumor metastasis. It has also been indicated LOXs have a noteworthy role in non-tumor diseases. Nonetheless, the role of LOXs in systemic or local organ development and disease control remains unknown. In the present study, the essential roles that LOXs play in embryogenesis were unveiled partially, whereas the role of LOXs in organ or systematic development requires further investigations. The present review aimed to discuss the roles of members of the LOX family in the context of the remodeling of organogenesis and organ development. In addition, the consequences of the malfunction of these proteins related to the development of abnormalities and resulting diseases is discussed. Contents 1. Introduction 2. Roles of members of the LOX family in organ development 3. Signaling pathways involved in the modulation of LOX during tissue development 4. Conclusion Andrology Laboratory and

Hepatic stellate cells-specific LOXL1 deficiency abrogates hepatic inflammation, fibrosis, and corrects lipid metabolic abnormalities in non-obese NASH mice

“…Under physiological conditions, formation of ECM crosslinking play an important role in maintaining tissue structure and regulating cellular function. For example, LOX knockout mice died perinatal due to aortic aneurysms, cardiovascular dysfunction and diaphragmatic ruptures (26,27); LOXL1 de ciency induces a strong phenotype in mice with disturbance of elastic ber (28)(29)(30); general LOX inhibitor usually decreases the amount of several collagen and elastin cross-links, however it is not always able to restore tissue architecture as shown in a hyperoxia-based mouse model of bronchopulmonary dysplasia associated with aberrant late lung development (31). Recently, using Loxl1 knockout mice, Li et al found that living Loxl1 knockout mouse eyes, ocular compliance in Loxl1 knockout mice was lower than wild-type littermates (32).…”

Hepatic stellate cells-specific Loxl1 deficiency abrogates hepatic inflammation, fibrosis, and corrects lipid metabolic abnormalities in non-obese NASH mice

“…Under physiological conditions, formation of ECM crosslinking play an important role in maintaining tissue structure and regulating cellular function. For example, LOX knockout mice died perinatal due to aortic aneurysms, cardiovascular dysfunction and diaphragmatic ruptures (26, 27); LOXL1 de ciency induces a strong phenotype in mice with disturbance of elastic ber (28-30); general LOX inhibitor usually decreases the amount of several collagen and elastin cross-links, however it is not always able to restore tissue architecture as shown in a hyperoxia-based mouse model of bronchopulmonary dysplasia associated with aberrant late lung development (31). Recently, using Loxl1 knockout mice, Li et al found that living Loxl1 knockout mouse eyes, ocular compliance in Loxl1 knockout mice was lower than wild-type littermates (32).…”

Diagnostic Value, Prognostic Value, and Immune Infiltration of LOX Family Members in Liver Cancer: Bioinformatic Analysis

“…Previous studies have demonstrated that LOX is highly expressed in the fibrous lamina propria in the small intestine, stomach, and liver, as well as other tissues that contain elastic fibers and fibrillar collagen (16). LOX, LOXL, LOXL2, LOXL3 and LOXL4 were to be in intracellular locations, perinuclear regions and intranuclear locations, and are secreted to exert their functions, such as extracellular enzyme for initiating covalent cross-link formation in collagen fibrils (15,19,(32)(33)(34)(35). After secretion, LOX family members oxidase crosslink collagen and elastin (19,36).…”