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Last update 08 May 2025

MIR29B1

Last update 08 May 2025

Basic Info

Synonyms

hsa-mir-29b-1, microRNA 29b-1, MIR29B1

+ [1]

Introduction-

Drugs associated with MIR29B1

BNC-1602

Target

MIR29B1

Mechanism

MIR29B1 inhibitors [+1]

Active Org.

BONAC Corp.

Originator Org.

BONAC Corp.

Active Indication

Liver Cirrhosis [+1]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

AAV-miR-29b

Target

MIR29B1 x MIR29B2

Mechanism

MIR29B1 inhibitors [+1]

Active Org.

Jichi Medical University

Originator Org.

Jichi Medical University

Active Indication

Stomach Cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MIR29B1

100 Translational Medicine associated with MIR29B1

0 Patents (Medical) associated with MIR29B1

1,227

Literatures (Medical) associated with MIR29B1

01 Sep 2025·Neural regeneration research

Acquired sensorineural hearing loss, oxidative stress, and microRNAs.

Article

Author: Guo, Ru C ; Nunez, Desmond A

Hearing loss is the third leading cause of human disability. Age-related hearing loss, one type of acquired sensorineural hearing loss, is largely responsible for this escalating global health burden. Noise-induced, ototoxic, and idiopathic sudden sensorineural are other less common types of acquired hearing loss. The etiology of these conditions is complex and multi-factorial involving an interplay of genetic and environmental factors. Oxidative stress has recently been proposed as a likely linking cause in most types of acquired sensorineural hearing loss. Short non-coding RNA sequences known as microRNAs (miRNAs) have increasingly been shown to play a role in cellular hypoxia and oxidative stress responses including promoting an apoptotic response. Sensory hair cell death is a central histopathological finding in sensorineural hearing loss. As these cells do not regenerate in humans, it underlies the irreversibility of human age-related hearing loss. Ovid EMBASE, Ovid MEDLINE, Web of Science Core Collection, and ClinicalTrials.gov databases over the period August 1, 2018 to July 31, 2023 were searched with "hearing loss," "hypoxamiRs," "hypoxia," "microRNAs," "ischemia," and "oxidative stress" text words for English language primary study publications or registered clinical trials. Registered clinical trials known to the senior author were also assessed. A total of 222 studies were thus identified. After excluding duplicates, editorials, retractions, secondary research studies, and non-English language articles, 39 primary studies and clinical trials underwent full-text screening. This resulted in 11 animal, in vitro , and/or human subject journal articles and 8 registered clinical trial database entries which form the basis of this narrative review. MiRNAs miR-34a and miR-29b levels increase with age in mice. These miRNAs were demonstrated in human neuroblastoma and murine cochlear cell lines to target Sirtuin 1/peroxisome proliferator-activated receptor gamma coactivator-1-alpha (SIRT1/PGC-1α), SIRT1/p53, and SIRT1/hypoxia-inducible factor 1-alpha signaling pathways resulting in increased apoptosis. Furthermore, hypoxia and oxidative stress had a similar adverse apoptotic effect, which was inhibited by resveratrol and a myocardial inhibitor-associated transcript, a miR-29b competing endogenous mRNA. Gentamicin reduced miR-182-5p levels and increased cochlear oxidative stress and cell death in mice - an effect that was corrected by inner ear stem cell-derived exosomes. There is ongoing work seeking to determine if these findings can be effectively translated to humans.

01 Jul 2025·European Journal of Pharmacology

Effects of maternal smoking on inflammation, autophagy/mitophagy, and miRNAs in endothelial cells: Influence of newborn sex

Article

Author: Montella, Andrea ; Lodde, Valeria ; Franconi, Flavia ; Criscione, Massimo ; Campesi, Ilaria ; Capobianco, Giampiero

Maternal smoking (MS) during pregnancy is linked to well-documented adverse health effects for the mother and foetus, however the role of fetal sex was largely overlooked. Primary cultures of male and female human umbilical vein endothelial cells (MHUVECs and FHUVECs, respectively) were used. IL-6, IL-8, and TNF-α levels were measured in HUVECs supernatant. The expression of genes and proteins (oestrogen receptors (ERs), Hsp90, Beclin-1, p62, LC3, LAMP-1 and Parkin), as well as the expression of miR-29a-3p, miR-29b-3p, miR-126-3p, miR-133a-3p, and miR-146a-5p were analysed in cells obtained from foetuses born to non-smoking and smoking mothers. In HUVECs from foetuses born to non-smoking mothers, Beclin-1 protein was higher in MHUVECs (1.8 fold increase), while Parkin, Hsp90 proteins, and miR-146a-5p were elevated in FHUVECs (2.2, 2.6, and 2.1 fold increase, respectively), with no other significant differences. MS amplified these sex differences, with specific effects based on foetus sex. FHUVECs obtained from foetus born to smoking mothers showed higher levels of IL-8 (1399.36 ± 123.96 pg/ml for FHUVECs vs 655.11 ± 215.94; pg/ml for MHUVECs; P < 0.001), Hsp90 gene and protein (3.3 and 2.6 fold increase), and ERβ protein and Beclin-1 gene (2.1, and 4.9 fold increase), and lower levels of miR-29b-3p, miR-133a-3p, and miR-146a-5p than MHUVECs (0.27, 0.68, and 0.1 fold change, respectively). This study shows that primary HUVECs from fetuses born to smoking mothers retain a memory of smoking effects, with sex differences in gene expression, miRNA profiles, and autophagic responses, suggesting that maternal smoking impacts endothelial cell physiology in a sex-dependent manner.

01 Jun 2025·Free Radical Biology and Medicine

Senescent cartilage endplate stem cells-derived exosomes induce oxidative stress injury in nucleus pulposus cells and aggravate intervertebral disc degeneration by regulating FOXO3

Article

Author: Li, Hao ; Liu, Chao ; Hu, Zhilei ; Wang, Siya ; Bian, Zhiqun ; Ouyang, Jian ; Zhang, Chao ; Liu, Minghan ; Wang, Tianling ; Zhang, Yuyao ; Li, Changqing ; Zhai, Yu ; Chang, Xian

Intervertebral disc degeneration (IVDD) is the leading cause of low back pain and associated disability worldwide. The cartilage endplate (CEP) is a critical structure in maintaining the homeostasis of the intervertebral disc, by exosomes (Exos)-mediated intracellular communication between cartilage endplate stem cells (CESCs) and nucleus pulposus cells (NPCs). However, whether the senescence of CESCs influences the functionality of CESCs-derived Exos (CESCs-Exos) and participates in the progress of IVDD remains unclear. In this study, we explored the role and mechanism of the Exos-based intracellular communication between senescent CESCs and NPCs in IVDD. CESCs isolated from aged individuals (S-CESCs) exhibited high levels of senescence compared with CESCs isolated from young individuals (Y-CESCs). Exos from Y-CESCs (Y-Exos) and from S-CESCs (S-Exos) were extracted and identified. Surprisingly, we found that S-Exos lost the therapeutic effects as the Y-Exos exhibited in mitigating IVDD, and even aggravated IVDD by inducing oxidative stress injury in NPCs. MicroRNA-sequencing revealed significant upregulation of miR-29b-3p expression in S-Exos. Through microRNA target prediction, dual luciferase assays, RNA-sequencing, lentivirus-mediated overexpression and suppression, we demonstrated that miR-29b-3p regulates the expression of FOXO3 and downstream antioxidant enzymes to induce oxidative stress injury in NPCs. In vivo experiments further verified that countering miR-29b-3p by antagomir reversed the detrimental effects of S-Exos in exacerbating IVDD. This work elucidates the role and mechanism of senescent CESCs in disrupting redox homeostasis in the nucleus pulposus and exacerbating IVDD by Exos-mediated intracellular communication and offers an experimental foundation for the selection of proper CESCs-Exos to obtain better therapeutic effects in IVDD.

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MIR29B1

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