ReviewInternational journal of molecular sciences2018
Ambiguous Effects of Autophagy Activation Following Hypoperfusion/Ischemia.
Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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
29 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- S-Propargyl-Cysteine Attenuates Stroke Heterogeneity via Promoting Protective Autophagy Across Multiple Neural Cell Types: Insights From Single-Cell Sequencing.CNS neuroscience & therapeutics · 2025Article
- Within the Ischemic Penumbra, Sub-Cellular Compartmentalization of Heat Shock Protein 70 Overlaps with Autophagy Proteins and Fails to Merge with Lysosomes.Molecules (Basel, Switzerland) · 2022Article
- Blockade on Lin28a Prevents Cognitive Impairment and Disruption of the Blood-Brain Barrier Induced by Chronic Cerebral Hypoperfusion.Biomedicines · 2022Article
- Melatonin attenuates cerebral hypoperfusion-induced hippocampal damage and memory deficits in rats by suppressing TRPM7 channels.Saudi journal of biological sciences · 2022Article
- Autophagy in glaucoma pathogenesis: Therapeutic potential and future perspectives.Frontiers in cell and developmental biology · 2022Review
- The Autophagy-Related Organelle Autophagoproteasome Is Suppressed within Ischemic Penumbra.International journal of molecular sciences · 2021Article
- Autophagic Upregulation Is Cytoprotective in Ischemia/Reperfusion-Injured Retina and Retinal Progenitor Cells.International journal of molecular sciences · 2021Article
- Autophagy & Phagocytosis in Neurological Disorders and their Possible Cross-talk.Current neuropharmacology · 2021Review
- Merging the Multi-Target Effects of Phytochemicals in Neurodegeneration: From Oxidative Stress to Protein Aggregation and Inflammation.Antioxidants (Basel, Switzerland) · 2020Review
- Single-step genome-wide association study for social genetic effects and direct genetic effects on growth in Landrace pigs.Scientific reports · 2020Article
- Transcriptional block of AMPK-induced autophagy promotes glutamate excitotoxicity in nutrient-deprived SH-SY5Y neuroblastoma cells.Cellular and molecular life sciences : CMLS · 2020Article
- Autophagy is a pro-survival adaptive response to heat shock in bovine cumulus-oocyte complexes.Scientific reports · 2020Article
- Autophagy in trimethyltin-induced neurodegeneration.Journal of neural transmission (Vienna, Austria : 1996) · 2020Review
- New Insights for nicotinamide: Metabolic disease, autophagy, and mTOR.Frontiers in bioscience (Landmark edition) · 2020Review
- Promiscuous Roles of Autophagy and Proteasome in Neurodegenerative Proteinopathies.International journal of molecular sciences · 2020Review
- mTOR-Related Cell-Clearing Systems in Epileptic Seizures, an Update.International journal of molecular sciences · 2020Review
- Natural Compounds and Autophagy: Allies Against Neurodegeneration.Frontiers in cell and developmental biology · 2020Review
- Role of Mitofusins and Mitophagy in Life or Death Decisions.Frontiers in cell and developmental biology · 2020Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Autophagy primarily works to counteract nutrient deprivation that is strongly engaged during starvation and hypoxia, which happens in hypoperfusion. Nonetheless, autophagy is slightly active even in baseline conditions, when it is useful to remove aged proteins and organelles. This is critical when the mitochondria and/or proteins are damaged by toxic stimuli. In the present review, we discuss to that extent the recruitment of autophagy is beneficial in counteracting brain hypoperfusion or, vice-versa, its overactivity may per se be detrimental for cell survival. While analyzing these opposite effects, it turns out that the autophagy activity is likely not to be simply good or bad for cell survival, but its role varies depending on the timing and amount of autophagy activation. This calls for the need for an appropriate autophagy tuning to guarantee a beneficial effect on cell survival. Therefore, the present article draws a theoretical pattern of autophagy activation, which is hypothesized to define the appropriate timing and intensity, which should mirrors the duration and severity of brain hypoperfusion. The need for a fine tuning of the autophagy activation may explain why confounding outcomes occur when autophagy is studied using a rather simplistic approach.
Indexed as
Identifiers
What Socratic 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 Socratic graph.