Acetyl-coenzyme A: a metabolic master regulator of autophagy and longevity.
Level 5 - mechanism / opinion, no new human data
Narrative commentary and mechanism-based reasoning summarizing preclinical bench research.
PubMed 24904996 · doi:10.4161/auto.28919
What was done
The authors review and synthesize findings regarding the role of nucleo-cytosolic acetyl-coenzyme A as an endogenous metabolic regulator of autophagy and aging across phylogenetically distinct model systems, specifically yeast and mammalian cells.
What was found
The abstract reports no numerical values or statistical effect sizes. It reports that nucleo-cytosolic acetyl-coenzyme A is the sole acetyl-group donor for protein acetylation, and that acetylation of histones and cytosolic proteins inversely correlates with the rate of autophagy in yeast and mammalian cells.
Why it matters
The paper proposes a conserved biochemical mechanism where acetyl-coenzyme A acts as a metabolic rheostat linking nutrient availability to autophagy suppression via protein acetylation.
Limits
The abstract represents a narrative commentary based on preclinical laboratory research rather than an empirical clinical trial. It provides no sample sizes, quantitative measurements, effect sizes, or human in vivo data.
Cited by
- supports Depleting glucose, amino acids, or fatty acids lowers cytosolic acetyl-CoA levels, which causes cytosolic protein deacetylation and stimulates autophagy.