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Last update 08 May 2025

MSMO1

Last update 08 May 2025

Basic Info

Synonyms

C-4 methylsterol oxidase, DESP4, ERG25

+ [4]

Introduction

Catalyzes the three-step monooxygenation required for the demethylation of 4,4-dimethyl and 4alpha-methylsterols, which can be subsequently metabolized to cholesterol (PubMed:21285510, PubMed:23583456, PubMed:26114596, PubMed:28673550). Also involved in drug metabolism, as it can metabolize eldecalcitol (ED-71 or 1alpha,25-dihydroxy-2beta-(3-hydroxypropoxy)-cholecalciferol), a second-generation vitamin D analog, into 1alpha,2beta,25-trihydroxy vitamin D3; this reaction occurs via enzymatic hydroxylation and spontaneous O-dehydroxypropylation (PubMed:26038696).

Drugs associated with MSMO1

PF-1163A

Target

MSMO1

Mechanism

MSMO1 inhibitors

Active Org.

Meiji Seika Pharma Ltd.

Originator Org.

Meiji Seika Pharma Co., Ltd.

Active Indication

Mycoses

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

PF-1163B

Target

MSMO1

Mechanism

MSMO1 inhibitors

Active Org.-

Originator Org.

Meiji Seika Pharma Ltd.

Active Indication-

Inactive Indication

Mycoses

Drug Highest PhaseDiscontinued

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MSMO1

100 Translational Medicine associated with MSMO1

0 Patents (Medical) associated with MSMO1

179

Literatures (Medical) associated with MSMO1

01 Jun 2025·Toxicon

The DHCR7 is the key target of lipotoxic liver injury caused by matrine through abnormal activation of the cholesterol synthesis pathway

Article

Author: Li, Jiaqi ; Zhang, Wenting ; Tao, Xiaoyu ; Li, Zhiqi ; Zhao, Chongjun ; Fan, Qiqi ; Gao, Yifei ; Chen, Linzhen ; Wu, Jiarui ; Lu, Shan

BACKGROUNDMatrine, the main active ingredient in Sophora flavescens and Sophorae tonkinensis radix et rhizome, is a highly effective insecticide. However, its hepatotoxicity to some extent affects its application value. This study aimed to explore the mechanism underlying matrine-induced liver injury.METHODSThe zebrafish (Danio rerio) and L02 cell model were utilized to investigate the toxic dose of matrine and its effects on liver tissue damage, liver cell morphology and activity, and expression levels of ALT and AST. Zebrafish and L02 cell samples were then collected for transcriptomic testing to further explore the possible mechanism by which matrine induced liver injury. Finally, integrated bioinformatics methods and experiments were used to elucidate the possible mechanisms behind matrine-induced liver injury.RESULTSThe result presented solid in vivo evidence of matrine-induced hepatotoxicity, supported by abnormal changes of liver morphological, disturbed liver cell structure, obvious apoptosis, as well as elevated levels of ALT and AST in zebrafish. In addition, in vitro L02 cell experiments also showed that matrine can produce significant liver cell damage effects. The integrated bioinformatics analysis results revealed that differentially expressed genes (DEGs) were substantially enriched in multiple pathways related to lipid regulation. Among which, the steroid biosynthesis was the most key signaling pathway, evidenced by the enhanced expression of eight genes, including DHCR7, SQLE, CYP51, CYP24A1, SC5D, LSS, MSMO1 and SOAT1. Furthermore, AY9944, the targeted inhibitor of DHCR7, could offset the toxic effect, as reflected by diminished liver phenotype damage, steatosis, and cholesterol accumulation caused by matrine.CONCLUSIONSMatrine can upregulate the expression of key genes in steroid biosynthesis pathway, resulting in cholesterol accumulation and then inducing hepatotoxicity. Among them, targeted inhibition of DHCR7 gene expression can alleviate matrine-induced liver injury.

11 Apr 2025·Investigative Ophthalmology & Visual Science

Treatment of Pathological Lymphangiogenesis via Circular RNA-Mediated Cholesterol Metabolism Remodeling

Article

Author: Jiang, Qin ; Zhang, Ziran ; Mu, Wan ; Shi, Lianjun ; Yan, Biao ; Ye, Fan ; Liu, Qian ; Li, Xiumiao ; Lu, Shuting

PurposeLymphangiogenesis plays important roles in the pathogenesis of human diseases, including inflammatory ocular diseases, metabolic diseases, and cancers, by affecting lipid metabolism and immune homeostasis. Despite growing evidence showing that circular RNAs (circRNAs) act as the regulators of inflammatory and metabolic pathways, their roles in lymphatic dysfunction remain unclear. This study aims to explore the involvement of circRNA-KIF6 (cKIF6) in pathological lymphangiogenesis and elucidate the underlying mechanism.MethodsThe cKIF6 expression was evaluated in mouse-sutured corneas and lymphatic endothelial cells (LECs) isolated from juvenile foreskin under inflammatory conditions. Functional assays, including viability, proliferation, migration, and tube formation, were conducted on LECs after cKIF6 silencing. Lymphangiogenesis was evaluated using mouse-sutured cornea and Matrigel plug models. Mechanistic studies explored the role of cKIF6 as a molecular sponge for miR-582 and its downstream effect on methylsterol monooxygenase 1 (MSMO1).ResultsThe cKIF6 expression was significantly elevated in mouse-sutured corneas and inflamed LECs. Silencing cKIF6 impaired LEC viability, proliferation, migration, and tube formation, leading to reduced lymphangiogenesis in both in vitro and in vivo models. Mechanistically, cKIF6 acted as a miR-582 sponge, resulting in elevated MSMO1 expression and increased cholesterol content in LECs. The augmented proliferation, migration, and tube formation abilities of cKIF6-overexpressing LECs were attenuated by the inhibitor of cholesterol biosynthesis.ConclusionsThe cKIF6 regulates lymphangiogenesis by targeting cholesterol metabolism, making it a promising therapeutic target for lymphangiogenesis-related diseases.

01 Mar 2025·Poultry Science

Integrated metabolome and transcriptome analysis reveals key genes and pathways associated with egg yolk percentage in chicken

Article

Author: Luo, Yuxing ; Zhu, Shoujia ; Zhao, Xuli ; Ning, Zhonghua ; Wang, Mengyuan ; Li, Wen

Yolk percentage is a critical index in the egg product industry, reflecting both nutritional value and economic benefits. To elucidate the underlying mechanisms that contribute to variations in egg yolk percentage, we performed integrated transcriptome and metabolome analyses on the liver, ovary, and magnum tissues of Rhode Island Red chickens with high and low yolk percentages. A total of 322 differentially expressed genes (DEGs) and 128 significantly differential metabolites (SDMs) (VIP>1, P < 0.05) were identified in the liver, whereas 419 DEGs and 215 SDMs were detected in the ovary, and 238 DEGs along with 47 SDMs were found in the magnum. In the liver, genes such as HMGCR, DHCR7, MSMO1, and CYP7A1 were linked to cholesterol metabolism, essential for steroid hormone synthesis and yolk formation, while ACACB, ACSL1, ACSL4, LPL, and SGPP2 were involved in fatty acid biosynthesis, a key process for supplying energy and structural components of the yolk. In the ovary, COL6A6, COMP, CHAD, ITGA7, THBS2, and TNC contributed to extracellular matrix-receptor interactions, which are fundamental for follicle development and oocyte maturation. In the magnum, UGT1A1, MAOB, and ALDH3B2 participated in drug metabolism-cytochrome P450 and amino acid metabolism, ensuring a proper environment for egg white formation and potentially influencing nutrient allocation to the yolk. Metabolic pathway enrichment revealed that steroid hormone biosynthesis, glycerophospholipid metabolism, and betaine metabolism were predominant in the liver; pyruvate, taurine, and hypotaurine metabolism in the ovary; and phenylalanine metabolism in the magnum. Moreover, integrated analysis highlighted key metabolites and genes potentially regulating yolk deposition, including 7,8-dihydroneopterin and Pg 38:4 in the liver (related to immune modulation and lipid metabolism, respectively), thalsimine in the ovary, as well as DL-glutamine in the magnum, all of which may be crucial for maintaining metabolic homeostasis and supporting egg formation. Collectively, these findings deepen our understanding of how distinct molecular and metabolic pathways in the liver, ovary, and magnum orchestrate yolk proportion and deposition. Such insights may advance future strategies to improve egg quality and productivity in poultry breeding programs.

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