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Last update 08 May 2025

miR-31

Last update 08 May 2025

Basic Info

Synonyms

hsa-mir-31, microRNA 31, MIR31

+ [1]

Introduction-

Drugs associated with miR-31

WO2023280001

Patent Mining

Target

miR-31

Mechanism-

Active Org.

Jinan University

Originator Org.

Jinan University

Active Indication

Hemic and Lymphatic Diseases [+1]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with miR-31

100 Translational Medicine associated with miR-31

0 Patents (Medical) associated with miR-31

991

Literatures (Medical) associated with miR-31

31 Dec 2025·Organogenesis

Correlation of MicroRNA-31 with Endometrial Receptivity in Patients with Repeated Implantation Failure of In Vitro Fertilization and Embryo Transfer

Article

Author: Tan, Yan ; Chen, Minhong ; Chen, Xixi ; Du, Bijun

OBJECTIVEThis trial probed the correlation between miR-31 expression and endometrial receptivity (ER) in patients with repeated implantation failure (RIF) of in vitro fertilization and embryo transfer (IVF-ET).METHODSA retrospective study of 80 infertility patients who underwent IVF-ET assisted conception treatment were divided into RIF group and normal pregnancy group (control group) according to the pregnancy outcome after embryo transfer. General information of both groups was collected. Endometrial tissues were collected in the middle luteal phase of the menstrual cycle before IVF-ET. miR-31 levels in endometrial tissues were measured, and endometrial tolerance indicator pulsatility index (PI), resistance index (RI), and endometrial thickness (Em) were detected. The correlation between endometrial miR-31 levels and ER indices was evaluated by Pearson method. ROC curves were utilized to analyze the efficacy of miR-31 in predicting RIF occurrence. The influencing factors of RIF were analyzed by binary Logistic regression.RESULTSRIF patients had increased miR-31 expression level and endometrial tolerance indicator PI, and RI while decreased Em (p < 0.05). miR-31 in RIF patients was positively correlated with PI and RI, and negatively correlated with Em (p < 0.05). The area under the curve for miR-31 to predict the occurrence of RIF was 0.899, with a sensitivity of 0.750 and a specificity of 0.950. PI, RI, and miR-31 were risk factors for developing RIF in IVF-ET women, and Em was a protective factor (p < 0.05).CONCLUSIONmiR-31 in RIF patients is positively correlated with PI and RI, and negatively correlated with Em.

01 Jun 2025·Biochemistry and Biophysics Reports

Hsa-miR-31-3p targets CLDN8 to compromise skin barrier integrity in psoriasis

Article

Author: He, Li ; Tu, Yunhua ; Wang, Li ; An, Lijun

Skin barrier dysfunction in psoriasis has emerged as a significant concern, yet the underlying molecular mechanisms remain incompletely understood. This study investigates the role of hsa-miR-31-3p in regulating skin barrier function through its interaction with claudin-8 (CLDN8) in psoriasis. Through analysis of clinical samples and public datasets, we observed significantly impaired skin barrier function in psoriasis patients, characterized by increased transepidermal water loss and decreased stratum corneum hydration. Notably, CLDN8 expression was markedly downregulated in psoriatic lesions, while hsa-miR-31-3p levels were elevated. Bioinformatics analysis and molecular studies revealed that hsa-miR-31-3p directly targets the 3'UTR of CLDN8, leading to its downregulation. In vitro experiments demonstrated that both CLDN8 knockdown and hsa-miR-31-3p overexpression compromised the permeability barrier in keratinocytes. Furthermore, in an imiquimod-induced psoriasis mouse model, administration of mmu-miR-31-3p antagomir effectively ameliorated skin barrier damage, reduced inflammatory manifestations, and restored CLDN8 expression. These findings unveil a novel mechanism whereby hsa-miR-31-3p regulates skin barrier function through CLDN8 in psoriasis, suggesting potential therapeutic strategies targeting this pathway for psoriasis treatment.

01 Jun 2025·Journal of Translational Autoimmunity

The role of UV-induced cutaneous matrix metalloproteinases and mi-RNAs in the pathogenesis of lupus erythematosus

Article

Author: Niebel, D ; Berneburg, M ; Kurz, B ; Svilenska, T ; Karrer, S ; Ivanova, I ; Maisch, T

Cutaneous (CLE) and systemic lupus erythematosus (SLE) are autoimmune diseases with a multifactorial pathogenesis. Ultraviolet radiation (UVR) is the most important trigger of CLE; however, the degree of photosensitivity varies between the clinical subtypes. The expression of matrix metalloproteinases (MMPs)-important enzymes involved in skin turnover and homeostasis-is modulated by UVR. To investigate the causality of the clinically observed effects of UVR, sun-exposed lesional skin samples from patients with different subtypes of lupus erythematosus (LE) were examined by immunohistochemistry for the expression of MMP1 and MMP28 and compared with biopsies from polymorphous light eruption (PLE) and healthy skin (HS). The expression of micro-RNAs (miR-31 and miR-150)-regulators of MMP expression and cellular metabolism-in the samples was determined by in-situ hybridization and correlated with the expression of the glucose transporter 1 (GLUT1) receptor to examine potential metabolic regulation. To assess potential UVR regulation of MMP28, we performed in vitro experiments in healthy keratinocytes and fibroblasts. MMP28 expression was differentially affected by UVA1 and UVB irradiation in keratinocytes and fibroblasts. Compared with all other LE subtypes, as well as PLE and HS samples, MMP28 expression in Chilblain LE skin showed a distinct vertical distribution, reaching as far as the upper layers of the dermis. This vertical expression pattern coincided with decreased GLUT1 levels and with increased expression of miR-31 and miR-150 in the epidermis of patients with Chilblain LE. These data provide evidence for a potential metabolic dysregulation that may play a role in the etiology of LE. Furthermore, our results suggest MMP28 as a novel complementary marker in Chilblain LE diagnosis.

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miR-31

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