ArticleCell systems2023
Context-dependent regulation of lipid accumulation in adipocytes by a HIF1α-PPARγ feedback network.
Article in Cell systems, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Targeting the HIF-1α/PPARγ axis with curcumin carbon dots to combat uranium nephrotoxicity.Journal of nanobiotechnology · 2026Article
- AMPK in charge: aerobic glycolysis programs unilocularity in adipocytes.Journal of lipid research · 2026Article
- HIF1α reinforces PPARγ-dependent metabolic rechanneling to support lipid accumulation in adipocytes.Frontiers in molecular medicine · 2026Article
- Hypoxic microenvironment and pulmonary hypertension.Respiratory research · 2025Review
- Integrated multi‑omics analysis of liver metabolic dysregulation in ACE2 knockout mice.International journal of molecular medicine · 2025Article
- Specific muscle targeted delivery of miR-130a loaded lipid nanoparticles: a novel approach to inhibit lipid accumulation in skeletal muscle and obesity.Journal of nanobiotechnology · 2025Article
- Deciphering the anti-obesity mechanisms of pharmabiotic probiotics through advanced multiomics analysis.iScience · 2025Article
- Physiology-informed regularisation enables training of universal differential equation systems for biological applications.PLoS computational biology · 2025Article
- Contribution of glucose and glutamine to hypoxia-induced lipid synthesis decreases, while contribution of acetate increases, during 3T3-L1 differentiation.Scientific reports · 2024Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Hypoxia-induced upregulation of HIF1α triggers adipose tissue dysfunction and insulin resistance in obese patients. HIF1α closely interacts with PPARγ, the master regulator of adipocyte differentiation and lipid accumulation, but there are conflicting results regarding how this interaction controls the excessive lipid accumulation that drives adipocyte dysfunction. To directly address these conflicts, we established a differentiation system that recapitulated prior seemingly opposing observations made across different experimental settings. Using single-cell imaging and coarse-grained mathematical modeling, we show how HIF1α can both promote and repress lipid accumulation during adipogenesis. Our model predicted and our experiments confirmed that the opposing roles of HIF1α are isolated from each other by the positive-feedback-mediated upregulation of PPARγ that drives adipocyte differentiation. Finally, we identify three factors: strength of the differentiation cue, timing of hypoxic perturbation, and strength of HIF1α expression changes that, when considered together, provide an explanation for many of the previous conflicting reports.
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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 OpenQuestion graph.