ReviewBiochimica et biophysica acta2014
Regulation of autophagy and mitophagy by nutrient availability and acetylation.
Review in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 2 of them syntheses 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
43 citing papers in PubMed, 2 syntheses or guidelines pooled it, 69 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition).Autophagy · 2016Guideline
- Fasting and refeeding differentially regulate NLRP3 inflammasome activation in human subjects.The Journal of clinical investigation · 2015Trial
- Endogenous metabolite signaling orchestrates tumor immune evasion.Cell insight · 2026Review
- Article
- The intrinsically disordered regions of organellophagy receptors are interchangeable and control organelle fragmentation, ER-phagy and mitophagy flux.Nature cell biology · 2025Article
- RNA-seq analysis of mitochondria-related genes regulated by AMPK in the human trophoblast cell line BeWo.Animal models and experimental medicine · 2025Article
- Time Restricted Eating: A Valuable Alternative to Calorie Restriction for Addressing Obesity?Current obesity reports · 2025Review
- T cell exhaustion in malignant gliomas.Trends in cancer · 2023Review
- The endo-lysosomal regulatory protein BLOC1S1 modulates hepatic lysosomal content and lysosomal lipolysis.Biochemical and biophysical research communications · 2023Article
- Mitochondrial Autophagy in Ischemic Aged Livers.Cells · 2022Review
- Review
- AMPK Signaling Regulates Mitophagy and Mitochondrial ATP Production in Human Trophoblast Cell Line BeWo.Frontiers in bioscience (Landmark edition) · 2022Article
- All-Frontiers in oncology · 2022Article
- Renalase Challenges the Oxidative Stress and Fibroproliferative Response in COVID-19.Oxidative medicine and cellular longevity · 2022Review
- BLOC1S1/GCN5L1/BORCS1 is a critical mediator for the initiation of autolysosomal tubulation.Autophagy · 2021Article
- Sarcopenia: Etiology, Nutritional Approaches, and miRNAs.International journal of molecular sciences · 2021Review
- Oxygen sensing, mitochondrial biology and experimental therapeutics for pulmonary hypertension and cancer.Free radical biology & medicine · 2021Article
- The emerging roles of GCN5L1 in mitochondrial and vacuolar organelle biology.Biochimica et biophysica acta. Gene regulatory mechanisms · 2021Review
- Sex and BNIP3 genotype, rather than acute lipid injection, modulate hepatic mitochondrial function and steatosis risk in mice.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Normal cellular function is dependent on a number of highly regulated homeostatic mechanisms, which act in concert to maintain conditions suitable for life. During periods of nutritional deficit, cells initiate a number of recycling programs which break down complex intracellular structures, thus allowing them to utilize the energy stored within. These recycling systems, broadly named "autophagy", enable the cell to maintain the flow of nutritional substrates until they can be replenished from external sources. Recent research has shown that a number of regulatory components of the autophagy program are controlled by lysine acetylation. Lysine acetylation is a reversible post-translational modification that can alter the activity of enzymes in a number of cellular compartments. Strikingly, the main substrate for this modification is a product of cellular energy metabolism: acetyl-CoA. This suggests a direct and intricate link between fuel metabolites and the systems which regulate nutritional homeostasis. In this review, we examine how acetylation regulates the systems that control cellular autophagy, and how global protein acetylation status may act as a trigger for recycling of cellular components in a nutrient-dependent fashion. In particular, we focus on how acetylation may control the degradation and turnover of mitochondria, the major source of fuel-derived acetyl-CoA.
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.