ReviewFrontiers in cell and developmental biology2020
RNA-Binding Proteins Implicated in Mitochondrial Damage and Mitophagy.
Review in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
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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
20 citing papers in PubMed, 29 citations in OpenAlex.
- TDP-43 loss-of-function triggers mitochondrial dysfunction and metabolic imbalance.Neural regeneration research · 2026Article
- Impaired Myogenic Differentiation Is a Shared Feature Across Genetic Myopathies.International journal of molecular sciences · 2026Review
- TDP-43: [GU]-ardian of the transcriptome.Molecular neurodegeneration · 2026Review
- Wnt/β-catenin Pathway Aggravates Renal Fibrosis by Activating PUM2 Transcription to Repress YME1L-mediated Mitochondrial Homeostasis.Biochemical genetics · 2025Article
- Hypothermia regulates mitophagy and apoptosis via PINK1/Parkin-VDAC 3 signaling pathway during oxygen-glucose deprivation/recovery injury.Scientific reports · 2025Article
- Regulation of DNA damage response by RNA/DNA-binding proteins: Implications for neurological disorders and aging.Ageing research reviews · 2024Review
- The axes of biology: a novel axes-based network embedding paradigm to decipher the functional mechanisms of the cell.Bioinformatics advances · 2024Article
- Advancements in mitochondrial-targeted nanotherapeutics: overcoming biological obstacles and optimizing drug delivery.Frontiers in immunology · 2024Review
- TDP-43 protein interactome informs about perturbed canonical pathways and may help develop personalized medicine approaches for patients with TDP-43 pathology.Drug discovery today · 2023Review
- RNA binding protein AUF1/HNRNPD regulates nuclear export, stability and translation ofOpen biology · 2023Article
- Editorial: RNA binding proteins in neuroscience.Frontiers in molecular neuroscience · 2023Article
- T-Cell Intracellular Antigen 1-Like Protein in Physiology and Pathology.International journal of molecular sciences · 2022Review
- Protein lifetimes in aged brains reveal a proteostatic adaptation linking physiological aging to neurodegeneration.Science advances · 2022Article
- Stress-Induced Membraneless Organelles in Eukaryotes and Prokaryotes: Bird's-Eye View.International journal of molecular sciences · 2022Review
- Article
- Transcriptomic Analysis of Dysregulated Genes of the nDNA-mtDNA Axis in a Mouse Model of Dilated Cardiomyopathy.Frontiers in genetics · 2022Article
- Role of Mitochondrial Protein Import in Age-Related Neurodegenerative and Cardiovascular Diseases.Cells · 2021Review
- Differentially Expressed Circular RNAs in Peripheral Blood Mononuclear Cells of Patients with Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2021Article
- Communication Pattern Changes Along With Declined IGF1 of Immune Cells in COVID-19 Patients During Disease Progression.Frontiers in immunology · 2021Article
- RNA-Binding Motif Protein 11 (RBM11) Serves as a Prognostic Biomarker and Promotes Ovarian Cancer Progression.Disease markers · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mitochondrial lifecycle comprises biogenesis, fusion and cristae remodeling, fission, and breakdown by the autophagosome. This cycle is essential for maintaining proper cellular function, and inhibition of any of these processes results in deterioration of bioenergetics and swift induction of apoptosis, particularly in energy-craving cells such as myocytes and neurons. Regulation of gene expression is a fundamental step in maintaining mitochondrial plasticity, mediated by (1) transcription factors that control the expression of mitochondrial mRNAs and (2) RNA-binding proteins (RBPs) that regulate mRNA splicing, stability, targeting to mitochondria, and translation. More recently, RBPs have been also shown to interact with proteins modulating the mitochondrial lifecycle. Importantly, misexpression or mutations in RBPs give rise to mitochondrial dysfunctions, and there is strong evidence to support that these mitochondrial impairments occur early in disease development, constituting leading causes of pathogenesis. This review presents key aspects of the molecular network of the disease-relevant RBPs, including transactive response DNA-binding protein 43 (TDP43), fused in sarcoma (FUS), T-cell intracellular antigen 1 (TIA1), TIA-related protein (TIAR), and pumilio (PUM) that drive mitochondrial dysfunction in the nervous system.
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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.