ArticleNature communications2025
Mitofusin 2 displays fusion-independent roles in proteostasis surveillance.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed.
- Effects of Mdivi‑1 on Mitochondrial Fission and Fusion Proteins in Hippocampal Granule Neurons in Kainate-Induced Injury.Bulletin of experimental biology and medicine · 2026Article
- Rebalancing mitochondrial dynamics restores succinate dehydrogenase activity and reduces succinate release in hepatocellular carcinoma.Journal of biomedical science · 2026Article
- Mitochondrial Dysfunction: From Molecular Mechanisms to Modern Approaches for Basic and Clinical Research.Biomedicines · 2026Review
- Hippocampal CA1 and CA2 dendritic compartment-specific differences in mitochondrial form and function.Progress in neurobiology · 2026Article
- Hyperplasia suppressor gene inhibits the progression of malignant meningioma via the Wnt/β-catenin signaling pathway.Translational cancer research · 2026Article
- miR-103a-3p contributes to diabetic retinopathy progression via suppressing MFN2.Diabetology & metabolic syndrome · 2026Article
- Cooperative Architecture of Mitochondrial Proteome Homeostasis.medRxiv : the preprint server for health sciences · 2026Article
- Mitochondrial dysfunction and lipid droplet dynamics in MASH: HSD17B13 as a therapeutic target.Frontiers in cell and developmental biology · 2026Review
- Mitofusin MFN2 acts as a molecular sensor preventing protein aggregation and mitophagy, with a protective effect against apoptosis in Charcot-Marie-Tooth type 2A disease.Autophagy reports · 2026Article
- Hippocampal cell- and circuit-specific differences in mitochondrial form and function.bioRxiv : the preprint server for biology · 2025Article
- HSAInternational journal of molecular sciences · 2025Article
- Charcot-Marie-Tooth type 2A variants of mitofusin 2 sensitize cells to apoptotic cell death.Journal of cell science · 2025Article
- Protein Homeostasis and Mitochondrial Quality Control in Neurodegeneration.WIREs mechanisms of diseaseReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
Abstract
Mitochondria are essential organelles and their functional state dictates cellular proteostasis. However, little is known about the molecular gatekeepers involved, especially in absence of external stress. Here we identify a role of MFN2 in quality control independent of its function in organellar shape remodeling. MFN2 ablation alters the cellular proteome, marked for example by decreased levels of the import machinery and accumulation of the kinase PINK1. Moreover, MFN2 interacts with the proteasome and cytosolic chaperones, thereby preventing aggregation of newly translated proteins. Similarly to MFN2-KO cells, patient fibroblasts with MFN2-disease variants recapitulate excessive protein aggregation defects. Restoring MFN2 levels re-establishes proteostasis in MFN2-KO cells and rescues fusion defects of MFN1-KO cells. In contrast, MFN1 loss or mitochondrial shape alterations do not alter protein aggregation, consistent with a fusion-independent role of MFN2 in cellular homeostasis. In sum, our findings open new possibilities for therapeutic strategies by modulation of MFN2 levels.
Indexed as
Identifiers
What OpenQuestion holds
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.