Gene Expression in Adipocytes During Obesity: Understanding Challenges and Future Prospects

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 10 March 2026 | Viewed by 723

Special Issue Editor


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Guest Editor
Institute for Physiology and Pathophysiology, Department of Pathophysiology, Johannes Kepler University Linz, 4020 Linz, Austria
Interests: aging; hypoxia; stem cells; cardiometabolic diseases

Special Issue Information

Dear Colleagues,

Gene expression in adipocytes plays a pivotal role in the development and progression of obesity and its associated metabolic complications. Adipose tissue, once viewed primarily as an energy storage organ, is now recognized as a highly dynamic endocrine organ that secretes numerous adipokines and cytokines, influencing systemic metabolism, inflammation, and insulin sensitivity. In obesity, adipocytes undergo significant changes in size, number, and functionality, leading to altered gene expression profiles that contribute to chronic low-grade inflammation and insulin resistance. Understanding these molecular alterations is crucial for unraveling the complex pathophysiology of obesity. However, research in this area faces significant challenges, including the heterogeneity of adipose tissue and the interplay between genetic predispositions and (micro-)environmental factors (e.g., hypoxia). Future prospects lie in employing advanced genomic and proteomic technologies, single-cell analysis, and computational modeling to dissect the intricate regulatory networks governing gene expression in adipocytes during obesity, ultimately paving the way for novel therapeutic interventions.

The objective of this Special Issue is therefore to shed light on adipocyte pathophysiology on a genetic basis. For this issue, both original research articles and reviews are welcome. Research areas may include (but are not limited to) the following:

  • Epigenetic modifications and transcription factors in adipocytes;
  • Uncovering depot-specific differences in gene expression patterns;
  • Therapeutic targeting of gene expression to ameliorate obesity.

We look forward to receiving your contributions.

Dr. Markus Mandl
Guest Editor

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Keywords

  • adipocytes
  • adipose tissue
  • obesity
  • hypoxia
  • transcription factor
  • metabolism
  • epigenetics

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Published Papers (1 paper)

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Research

23 pages, 8052 KB  
Article
The Capability to Undergo ACSL4-Mediated Ferroptosis Is Acquired During Brown-like Adipogenesis and Affected by Hypoxia
by Markus Mandl, Elisabeth Heuboeck, Peter Benedikt, Florian Huber, Olga Mamunchak, Sonja Grossmann, Michaela Kotnik, Esma Hamzic-Jahic, Charnkamal Singh Bhogal, Anna-Maria Lipp, Edeltraud Raml, Werner Zwerschke, Martin Wabitsch, Jakob Voelkl, Andreas Zierer and David Bernhard
Cells 2025, 14(16), 1247; https://doi.org/10.3390/cells14161247 - 13 Aug 2025
Viewed by 537
Abstract
Adipose tissue enlargement in obesity leads to hypoxia, which may promote premature aging. This study aimed to understand the hypoxic response in 3D cultures of SGBS cells, a model for brown-like adipose tissue expressing uncoupling protein 1 (UCP1). Single-nucleus RNA sequencing of SGBS [...] Read more.
Adipose tissue enlargement in obesity leads to hypoxia, which may promote premature aging. This study aimed to understand the hypoxic response in 3D cultures of SGBS cells, a model for brown-like adipose tissue expressing uncoupling protein 1 (UCP1). Single-nucleus RNA sequencing of SGBS organoids revealed a heterogeneous composition and sub-population-specific responses to hypoxia. The analysis identified a cluster of transcriptional repression, indicating dying cells, and implied a role of ferroptosis in this model. Further experiments with SGBS cells and white adipose tissue-derived stem/progenitor cells showed that Acyl-CoA synthetase long-chain family member 4 (ACSL4), a key enzyme in ferroptosis, is expressed only in the presence of browning factors. Hypoxia downregulated ACSL4 protein in SGBS organoids but induced an inflammaging phenotype. Analysis of brown-like epicardial adipose tissue from cardiac surgery patients revealed a significant positive correlation of ACSL4 mRNA with UCP1 and hypoxia-inducible pro-inflammatory markers, while ACSL4 protein appeared to be inversely correlated. In conclusion, this study demonstrates that adipocytes’ capability to undergo ACSL4-mediated ferroptosis is linked to brown-like adipogenesis, suggesting an opportunity to modulate ferroptotic signaling in adipose tissue. The dual role of hypoxia by inhibiting ACSL4 but promoting inflammaging indicates a relationship between ferroptosis and aging that warrants further investigation. Full article
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