The DOI matches its Crossref record; 179 of the 179 references it cites were found in a registry or an index.
JNK1 and IKKβ: molecular links between obesity and metabolic dysfunction
Abstract
Inflammation is thought to underlie the pathogenesis of many chronic diseases. It is now established that obesity results in a state of chronic low‐grade inflammation thought to contribute to several metabolic disorders' including insulin resistance and pancreatic islet dysfunction. The protein kinases JNK1 and IKKβ have been found to serve as critical molecular links between obesity, metabolic inflammation, and disorders of glucose homeostasis. The precise mechanisms of these linkages are still being investigated. However, as we discuss here, JNK1 and IKKβ are activated by almost all forms of metabolic stress that have been implicated in insulin resistance or islet dysfunction. Furthermore, both JNK1 and IKKβ are critically involved in the promotion of diet‐induced obesity, metabolic inflammation, insulin resistance, and β‐cell dysfunction. Understanding the molecular mechanisms by which JNK1 and IKKβ mediate obesity‐induced metabolic stress is likely to be of importance for the development of new treatments for a variety of obesity‐associated diseases.—Solinas, G., Karin, M. JNK1 and IKKβ: molecular links between obesity and metabolic dysfunction. FASEB J . 24, 2596–2611 (2010). www.fasebj.org
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“On the other hand, during a pathophysiological state, abundant evidence indicates that a large and sustained increase in ROS impairs insulin action, through the activation of stress signaling pathways (*i.e.,* MAPK and JNK) ([85](#B85), [154](#B154)), contributing to the pathogenesis of diet-induced insulin resistance ([67](#B67)).”
From Mitochondrial fatty acid oxidation in obesity (2013) · cites this paper as [154]
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2 retracted
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RetractedObesity is associated with macrophage accumulation in adipose tissue
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Inflammation and metabolic disorders
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Adipose Expression of Tumor Necrosis Factor-α: Direct Role in Obesity-Linked Insulin Resistance
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Self-citationObesity induces a phenotypic switch in adipose tissue macrophage polarization
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Inflammatory Mechanisms in Obesity
Gregor, M. F., & Hotamisligil, G. S. (2011) · Annual Review of Immunology · doi:10.1146/annurev-immunol-031210-101322 · Cited by 3,754
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Lumeng, C. N., & Saltiel, A. R. (2011) · Journal of Clinical Investigation · doi:10.1172/jci57132 · Cited by 2,319
Copps, K. D., & White, M. F. (2012) · Diabetologia · doi:10.1007/s00125-012-2644-8 · Cited by 1,017
“Solinas G, Karin M. JNK1 and IKKβ: molecular links between obesity and metabolic dysfunction.”
BackgroundInfluentialYuan, T., Yang, T., Chen, H., Fu, D., Hu, Y., Wang, J., Yuan, Q., Yu, H., Xu, W., & Xie, X. (2018) · Redox Biology · doi:10.1016/j.redox.2018.09.025 · Cited by 766
Metadata
- Authors
- Solinas, G., & Karin, M.
- Affiliations
- University of Fribourg (CH)
- University of California San Diego (US)
- Corresponding author
- Solinas, Giovanni
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2010-04-06
- Volume
- 24
- Issue
- 8
- Pages
- 2596-2611
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- OpenAlex
- W2127873334
- Cited by
- 347
- References
- 179
- Citations by year
- 2026: 8 · 2025: 12 · 2024: 13 · 2023: 15 · 2022: 18 · 2021: 20 · 2020: 15 · 2019: 28 · 2018: 28 · 2017: 27 · 2016: 29 · 2015: 31 · 2014: 23 · 2013: 32 · 2012: 28
- FWCI
- 2.91
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The FASEB Journal (publishedVersion)
- PubMed (publishedVersion)
- reroDoc Digital Library (submittedVersion)
- Funders
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (SNF31003A‐118172)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
- Keywords
- JNK1, IKKβ, obesity, metabolic inflammation, insulin resistance, beta-cell dysfunction, pancreatic islets, glucose homeostasis, metabolic stress, diet-induced obesity, low-grade inflammation
- MeSH terms
- Humans, Inflammation, Metabolic Diseases, Obesity, Mitogen-Activated Protein Kinase 8, I-kappa B Kinase
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