ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2018
LncRNA MT1DP Aggravates Cadmium-Induced Oxidative Stress by Repressing the Function of Nrf2 and is Dependent on Interaction with miR-365.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- Environmental cadmium exposure and the risk of kidney stones: a systematic review and dose-response meta-analysis.Frontiers in medicine · 2025Pooled it
- Mapping the MicroRNA Landscape of Cadmium Exposure: A Bibliometric and Bioinformatics Analysis of Molecular Targets and Regulatory Pathways.International journal of molecular sciences · 2026Review
- Metal-dependent regulated cell death: Molecular architecture and translational frontiers.iMeta · 2026Review
- Research progress on the mechanism of tumor cell ferroptosis regulation by epigenetics.Epigenetics · 2025Review
- The Role of SLC7A11 in Tumor Progression and the Regulation Mechanisms Involved in Ferroptosis.Cancer management and research · 2025Review
- Dysregulation of Long Non-coding RNAs-the Novel lnc in Metal Toxicity and Carcinogenesis.Current environmental health reports · 2024Review
- Ellagic Acid Reduces Cadmium Exposure-Induced Apoptosis in HT22 Cells via Inhibiting Oxidative Stress and Mitochondrial Dysfunction and Activating Nrf2/HO-1 Pathway.Antioxidants (Basel, Switzerland) · 2024Article
- SIRT5-Mediated Desuccinylation of RAB7A Protects Against Cadmium-Induced Alzheimer's Disease-Like Pathology by Restoring Autophagic Flux.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- An adaptive biodegradable zinc alloy with bidirectional regulation of bone homeostasis for treating fractures and aged bone defects.Bioactive materials · 2024Article
- Ferroptosis-Regulated Natural Products and miRNAs and Their Potential Targeting to Ferroptosis and Exosome Biogenesis.International journal of molecular sciences · 2024Review
- Article
- The epigenetic regulatory mechanisms of ferroptosis and its implications for biological processes and diseases.MedComm · 2023Review
- LncAABR07053481 inhibits bone marrow mesenchymal stem cell apoptosis and promotes repair following steroid-induced avascular necrosis.Communications biology · 2023Article
- Biochar and organic fertilizer drive the bacterial community to improve the productivity and quality ofFrontiers in microbiology · 2023Article
- The Effect of Oxidative Stress-Induced Autophagy by Cadmium Exposure in Kidney, Liver, and Bone Damage, and Neurotoxicity.International journal of molecular sciences · 2022Review
- Significant reduction of long non-coding RNAs expression in bipolar disorder.BMC psychiatry · 2022Article
- Epigenetic Regulation in Exposome-Induced Tumorigenesis: Emerging Roles of ncRNAs.Biomolecules · 2022Review
- Estradiol mediates the interaction of LINC01541 and miR-429 to promote angiogenesis of G1/G2 endometrioid adenocarcinomaFrontiers in oncology · 2022Article
- Mechanism of miR-365 in regulating BDNF-TrkB signal axis of HFD/STZ induced diabetic nephropathy fibrosis and renal function.International urology and nephrology · 2021Article
- Ferroptosis Holds Novel Promise in Treatment of Cancer Mediated by Non-coding RNAs.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although cadmium (Cd)-induced hepatoxicity is well established, pronounced knowledge gaps remain existed regarding the inherent cellular signaling that dictates Cd toxicity. Specifically, the molecular basis for determining the equilibrium between prosurvival and proapoptotic signaling remains poorly understood. Thus, it is recently revealed that long non-coding RNA (lncRNA) MT1DP, a pseudogene in the metallothionein (MT) family, promoted Cd-induced cell death through activating the RhoC-CCN1/2-AKT pathway and modulating MT1H induction. Here, first the dependency of MT1DP induction on MTF1, an important transcriptional factor in driving the mRNA expression of MT1 members is defined. Additionally, a bridge molecule between MT1DP and nuclear factor erythroid 2-related factor 2 (Nrf2) is established: miR-365. Mechanistically, MT1DP induction under Cd stress decreases the nuclear factor erythroid 2-related factor 2 (Nrf2) level to evoke oxidative stress through the elevation of miR-365, which acted to repress the Nrf2 level via direct binding to its 3'UTR. In contrast to the competing endogenous RNA (ceRNA) mechanism, a new mechanism is proposed: MT1DP elevated the miR-365 level though stabilizing its RNA via direct binding. Collectively, the combined data demonstrate a crucial role of MT1DP in reducing the Nrf2-mediated protection of cells, and this is dependent on the interplay with miR-365. Hence, the study further expands the knowledge of inducible endogenous lncRNA in modulating oxidative stress.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.