Role of autophagy in the regulation of adipose tissue biology
Romero M., Zorzano A.
Narrative Review, published in Cell Cycle (2019) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Narrative Review
- Journal
- Cell Cycle (2019)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 31135269
- PMCID
- PMC6592255
- DOI
- 10.1080/15384101.2019.1624110
- Citations
- 23
Abstract (original English)
Autophagy plays a key role in cellular homeostasis since it allows optimal cellular functioning and provides energy under conditions of stress. Initial is revealed that alterations of macroautophagy disturb adipogenic differentiation in cultured cells, and in mice, leading to a drastic reduction of adipose tissue depots. Nevertheless, more recent studies indicate that autophagy participates in the control of adipose tissue biology in a more complex manner. The protein TP53INP2 activates the formation of autophagosomes by binding to ATG8 proteins such as LC3 or GATE16, and its genetic elimination reduces but does not cancel this activity. TP53INP2 deficiency increases adipogenic differentiation and induces a gain in adiposity in the mouse. At the cellular level, TP53INP2 promotes the sequestration of the regulatory protein GSK3β in multivesicular bodies (MVBs) by a process that involves autophagic activity and the participation of the endosomal sorting complexes required for transport (ESCRT) machinery. Through this mechanism, TP53INP2 stabilizes and activates β-catenin, which in turn triggers the inhibition of adipogenesis. In summary, autophagic pathways provide a whole set of mechanisms that may regulate in an opposite way the biology of adipose tissue, and consequently, have a variable impact on the whole body adiposity. This concept may be extensible to other cell types.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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