ReviewMolecular neurobiology2014
Autophagy coupling interplay: can improve cellular repair and aging?
Review in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 15 citations in OpenAlex.
- Study on the Effects and Mechanisms of Resveratrol in Improving Cognitive Impairment in AβJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Article
- Natural compounds in the regulation of proteostatic pathways: An invincible artillery against stress, ageing, and diseases.Acta pharmaceutica Sinica. B · 2021Review
- Emerging Roles of Tripartite Motif-Containing Family Proteins (TRIMs) in Eliminating Misfolded Proteins.Frontiers in cell and developmental biology · 2020Review
- Discovery of a potent small molecule inhibiting Huntington's disease (HD) pathogenesis via targeting CAG repeats RNA and Poly Q protein.Scientific reports · 2019Article
- Gp78 E3 Ubiquitin Ligase: Essential Functions and Contributions in Proteostasis.Frontiers in cellular neuroscience · 2017Review
- Mahogunin Ring Finger-1 (MGRN1), a Multifaceted Ubiquitin Ligase: Recent Unraveling of Neurobiological Mechanisms.Molecular neurobiology · 2016Review
- Ubiquitin ligase ITCH recruitment suppresses the aggregation and cellular toxicity of cytoplasmic misfolded proteins.Scientific reports · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Regular protein synthesis is a needful and complex task for a healthy cell. Improper folding leads to the deposition of misfolded proteins in cells. Autophagy and ubiquitin-proteasome system (UPS) are the conserved intracellular degradation processes of eukaryotic cells. How exactly these two pathways cross talk to each other is unclear. We do not know how the impairment of autophagy or UPS leads to the disturbance in cellular homeostasis and contribute into cellular aging and neurodegeneration. Here in this review, we will focus on the functional interconnections of autophagy and UPS, and why their loss of function results in abnormal aggregation of misfolded proteotoxic species in cells. Finally, we enumerate and discuss the crucial inducers of autophagy pathways and elaborate their intersection steps, which have been considered to be advantageous in aging linked with the abnormal protein aggregation. The final goal of this review is to improve our current understanding about multifaceted properties and interactions of autophagy and UPS, which may provide new insights to identify novel therapeutic strategies for aging and neurodegenerative diseases.
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.