Cited by 59Adipokines, Inflammation, and Metabolic DiseasesAdipose Tissue and MetabolismCardiovascular Disease and Adiposity

The Interplay Between Oxidative Stress and Lipid Composition in Obesity-Induced Inflammation: Antioxidants as Therapeutic Agents in Metabolic Diseases

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Olivares-Vicente, Mariló, Herranz-López, María·2025·International Journal of Molecular Sciences

Abstract

Adipose tissue functions not only as a lipid storage depot but also as an active endocrine organ that regulates key physiological processes. In obesity, oxidative stress disrupts the molecular pathways for adipose tissue homeostasis, triggering chronic inflammation, tissue dysfunction, and metabolic disorders. This review explores the mechanisms by which lipid storage drives adipose tissue expansion, highlighting the detrimental effects of hypertrophy in promoting oxidative stress, inflammation, and insulin resistance. These processes can ultimately contribute to metabolic pathologies such as cardiovascular diseases and type 2 diabetes. We also discuss how lipid composition influences these pathways, acting as signaling molecules that activate inflammatory and oxidative stress-related signaling cascades. Additionally, we compile evidence from studies on individuals with obesity, identifying lipids, oxidative stress markers, and inflammatory mediators as potential biomarkers of metabolic dysfunction. Finally, we assess the therapeutic potential of antioxidants in mitigating the metabolic effects of obesity, focusing on their mechanisms of actions. By integrating these insights, this review aims to clarify the complex relationship between oxidative stress, lipid metabolism, and inflammation, and highlight the role of antioxidant molecules in addressing adipose tissue dysfunction in obesity.

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  • Excessive lipid accumulation increases oxidative stress and promotes alterations in mitophagy.

    “Excessive lipid accumulation has been reported to increase oxidative stress and promote alterations in mitophagy [40, 41].”

    From Dyslipidemia-Induced Mitochondrial Dysfunctions in the Brains Does Not Reach Pathological Levels in the ApoE-Knockout Mice (2026) · cites this paper as [41]

    The Introduction (page unavailable) says lipid overload induces oxidative stress in adipocytes. Section 5 (page unavailable) discusses mitophagy, but links enhanced mitophagy to reduced phosphatidylcholine metabolism in macrophages; it does not establish that excessive lipid accumulation alters mitophagy. (LLM, conf=0.85)

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Cited by

Sorted by citations

Authors
Olivares-Vicente, M., & Herranz-López, M.
Affiliations
  • Universitat de Miguel Hernández d'Elx (ES)
  • Instituto de Investigación, Desarrollo e Innovación en Biotecnología Sanitaria de Elche (IDiBE), Miguel Hernández University (UMH), 03202 Elche, Spain
Venue
International Journal of Molecular Sciences
Publisher
MDPI AG
Published
2025-09-02
Volume
26
Issue
17
Pages
8544
ISSN
1422-0067 (ISSN-L)
OpenAlex
W4413915672
Cited by
59
References
15
Citations by year
2026: 55 · 2025: 4
FWCI
8.02
Type
journal article
Language
en
Open access
Locations
  • International Journal of Molecular Sciences (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • PubMed Central (publishedVersion, cc-by)
Funders
  • Spanish Ministry of Economy and Competitiveness (PID2021-125188OB-C32, PROMETEO/2021/059)
  • Generalitat Valenciana (PID2021-125188OB-C32, PROMETEO/2021/059)
Topics
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
Keywords
oxidative stress, lipid composition, obesity, adipose tissue inflammation, adipose tissue hypertrophy, insulin resistance, lipid signaling, antioxidant therapeutics, type 2 diabetes, cardiovascular disease, adipose tissue endocrine function
MeSH terms
Adipose Tissue, Animals, Antioxidants, Humans, Inflammation, Metabolic Diseases, Obesity, Oxidative Stress, Lipid Metabolism

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