ArticleAutophagy2024
The NLRX1-SLC39A7 complex orchestrates mitochondrial dynamics and mitophagy to rejuvenate intervertebral disc by modulating mitochondrial Zn
Article in Autophagy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 56 citations in OpenAlex.
- The role of sleep and circadian rhythms in intervertebral disc degeneration.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2026Review
- NLRX1 emerges as the only observed essential regulator of the mPTP, challenging mPTP inhibition as a valid target of cardioprotection.Basic research in cardiology · 2026Review
- NLRX1 is a critical neutrophil checkpoint modulating ferroptosis and suppressing NETosis to attenuate joint damage in arthritis.Cell death and differentiation · 2026Article
- Ubiquitination-mediated degradation of NLRX1 drives metabolic vulnerability and accelerates intervertebral disc degeneration.Cell death and differentiation · 2026Article
- miR-4632-5p Alleviates Lumbar Disc Degeneration by Targeting MAP3K11: A Novel Role in Mitigating Nucleus Pulposus Cell Degeneration.Biochemical genetics · 2026Article
- Nuciferine-Loaded Lipid Nanoparticle Microneedles Alleviate Intervertebral Disc Degeneration by Restoring Nucleus Pulposus Cell Homeostasis.Pharmaceutics · 2026Article
- Antioxidant Proline Carbon Dot-Composited Poly(L-methionine) Hydrogel Restores Mitophagy to Alleviate Cellular Senescence in Intervertebral Disc Degeneration.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Mitochondria‑endoplasmic reticulum contact site nexus: Molecular integration, disease pathogenesis and therapeutic opportunities (Review).International journal of molecular medicine · 2026Review
- Itgb1-Mediated Stabilization of Vimentin Alleviates Excessive Mechanical Stress-Induced Nucleus Pulposus Cell Pyroptosis and Intervertebral Disc Degeneration via PINK1-Parkin-Dependent Mitophagy.Cell proliferation · 2026Article
- Microenvironment-educated MSC-EVs loaded injectable smart hydrogel for targeting senescent nucleus pulposus cells and inhibiting ferroptosis against intervertebral disc degeneration.Bioactive materials · 2026Article
- Epigenetic research methods and animal models for intervertebral disc degeneration (Review).Molecular medicine reports · 2026Review
- SENP1 mitigates intervertebral disc degeneration: mechanisms involving suppression of pyroptosis and apoptosis in nucleus pulposus cells.Journal of orthopaedic surgery and research · 2026Article
- TDP43 cytoplasmic mislocalization initiates mitochondrial dysfunction and intercellular senescence propagation in intervertebral disc degeneration.Experimental & molecular medicine · 2026Article
- Efficacy and Mechanisms of Duhuo Jisheng Decoction in Treating Intervertebral Disc Degeneration: A Network Pharmacology and Experimental Study.Current medical science · 2026Article
- Epigenetic H3K4me3 activation of miR-155-5p promotes intervertebral disc degeneration via autophagy and ageing in nucleus pulposus cells.Non-coding RNA research · 2026Article
- Crosstalk between mitophagy and breast cancer: mechanisms of action and clinical applications.Journal of cancer research and clinical oncology · 2026Review
- Mitochondrial dysfunction in the pathogenesis of intervertebral disc herniation: a mitochondrial related genome-wide Mendelian randomization analysis.Journal of translational medicine · 2026Article
- Mechanisms underlying the reversal of hypoxia-induced energy metabolic reprogramming in cardiomyocytes by Poria cocos triterpenoids: integrated regulation of mitochondrial dynamics and the autophagy-lysosomal pathway.Frontiers in cardiovascular medicine · 2026Article
- Revisiting intervertebral disc degeneration: lipid metabolism disorders as overlooked contributors to complex pathology.Frontiers in immunology · 2026Review
- Senescence-associated secretory phenotype: the "pathogenic" factor driving orthopedic degenerative diseases and its regulation.Frontiers in aging · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intervertebral disc degeneration (IDD) is the most critical pathological factor in the development of low back pain. The maintenance of nucleus pulposus (NP) cell and intervertebral disc integrity benefits largely from well-controlled mitochondrial quality, surveilled by mitochondrial dynamics (fission and fusion) and mitophagy, but the outcome is cellular context-dependent that remain to be clarified. Our studies revealed that the loss of NLRX1 is correlated with NP cell senescence and IDD progression, which involve disordered mitochondrial quality. Further using animal and in vitro tissue and cell models, we demonstrated that NLRX1 could facilitate mitochondrial quality by coupling mitochondrial dynamic factors (p-DNM1L, L-OPA1:S-OPA1, OMA1) and mitophagy activity. Conversely, mitochondrial collapse occurred in NLRX1-defective NP cells and switched on the compensatory PINK1-PRKN pathway that led to excessive mitophagy and aggressive NP cell senescence. Mechanistically, NLRX1 was originally shown to interact with zinc transporter SLC39A7 and modulate mitochondrial Zn
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.