ArticleCell death & disease2025
Activating PIK3CA mutation promotes overgrowth of adipose tissue via inhibiting lipophagy in macrodactyly.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Lipophagy and lipid droplets in neurodegeneration.Trends in pharmacological sciences · 2026Review
- Global research status and trends in macrodactyly research: Bibliometric and visualized analysis from 2005 to 2025.Medicine · 2026Article
- [Effectiveness analysis of tibial nerve transection with epineurial suture and division of common plantar digital nerve branches in treatment of congenital macrodactyly in children].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
Excessive proliferation and lipid accumulation of adipose tissue are the main pathological alterations in macrodactyly. Our previous studies found that macrodactyly exhibits abnormal lipid metabolism and inhibited autophagy, but the underlying mechanisms remain unclear. This study aims to investigate the regulatory mechanisms of autophagy in macrodactyly. The therapeutic impact and underlying mechanisms of autophagy on lipid accumulation, induced by a gain-of-function mutation of PIK3CA in macrodactyly, were assessed with respect to autophagy, lipid metabolism, oxidative stress, and deubiquitination. Autophagy deficiency resulting from PIK3CA mutation in macrodactyly led to excessive accumulation of adipose tissue. Lipid accumulation can be mitigated by inducing lipophagy of lipid droplets (LDs) in adipose derived stem cells of macrodactyly (Mac-ADSCs). The subsequent increase in free fatty acids (FFA) led to mitochondrial oxidative stress in Mac-ADSCs. Inducing autophagy exacerbated mitochondrial oxidative stress in Mac-ADSCs, thereby contributing to apoptosis. Additionally, the ablation of the deubiquitinase USP15 facilitated the degradation of LDs in Mac-ADSCs, through ubiquitin-dependent macrolipophagy. USP15 inhibitor reduced lipid accumulation in macrodactyly adipose tissue xenografts. In conclusion, activating PIK3CA mutation promotes excessive proliferation and lipid accumulation of Mac-ADSCs by inhibiting lipophagy. Targeted inhibition of USP15 may serve as a promising therapeutic approach for treating macrodactyly. A schematic illustrates that activating PIK3CA mutation promotes overgrowth of adipose tissue via inhibiting lipophagy in macrodactyly.
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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.