Jak-TGFβ cross-talk links transient adipose tissue inflammation to beige adipogenesis
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Transient inflammation in adipose tissue triggers Jak-TGFβ signaling to promote beige adipocyte differentiation.
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IL-6 signaling through STAT3 controls accelerated loss of white adipose tissue, as shown by inhibition of white adipose tissue lipolysis in mice treated with anti-IL-6R antibody.
“IL-6 signaling through STAT3 has been shown to control this process, as evidenced by inhibition of white adipose tissue lipolysis in mice treated with anti–IL-6R antibody”
From Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 To Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution (2020) · cites this paper as Babaei et al., 2018
The section on transient IL-6 family activation reports that lipolytic stimulation raises IL-6 and IL-11, activating Jak/Stat3 in adipocyte progenitors. The Discussion says Stat3 activation depended on lipolysis in this model, rather than showing that IL-6–STAT3 signaling controlled white adipose tissue loss. Our copy does not report inhibition of lipolysis in mice treated with anti–IL-6R antibody. (LLM, conf=0.84)
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Cites
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Bharadwaj, U., Kasembeli, M. M., Robinson, P., & Tweardy, D. J. (2020) · Pharmacological Reviews · doi:10.1124/pr.119.018440 · Cited by 314 · see citing works
“IL-6 signaling through STAT3 has been shown to control this process, as evidenced by inhibition of white adipose tissue lipolysis in mice treated with anti–IL-6R antibody (Babaei et al., 2018; Wang et al., 2018a).”
BackgroundInterleukin-6 released from differentiating human beige adipocytes improves browning
Kristóf, E., Klusóczki, Á., Veress, R., Shaw, A., Combi, Z. S., Varga, K., Győry, F., Balajthy, Z., Bai, P., Bacso, Z., et al. (2019) · Experimental Cell Research · doi:10.1016/j.yexcr.2019.02.015 · Cited by 77 · see citing works
Adipose tissue aging is regulated by an altered immune system
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Gutierrez, A. D., Gao, Z., Hamidi, V., Zhu, L., Saint Andre, K. B., Riggs, K., Ruscheinsky, M., Wang, H., Yu, Y., Miller, C., et al. (2022) · Cell Reports Medicine · doi:10.1016/j.xcrm.2022.100813 · Cited by 44 · see citing works
- Authors
- Babaei, R., Schuster, M., Meln, I., Lerch, S., Ghandour, R. A., Pisani, D. F., Bayindir-Buchhalter, I., Marx, J., Wu, S., Schoiswohl, G., Billeter, A. T., Krunic, D., Mauer, J., Lee, Y.-H., Granneman, J. G., Fischer, L., Müller-Stich, B. P., Amri, E.-Z., Kershaw, E. E., Heikenwälder, M., Herzig, S., & Vegiopoulos, A.
- Affiliations
- DKFZ Junior Group Metabolism and Stem Cell Plasticity (A171), German Cancer Research Center, Heidelberg 69120, Germany.
- German Cancer Research Center (DE)
- Centre National de la Recherche Scientifique (FR)
- University of Pittsburgh (US)
- Heidelberg University (DE)
- Max Planck Institute for Metabolism Research (DE)
- Yonsei University (KR)
- Wayne State University (US)
- Corresponding author
- Herzig, Stephan
- Vegiopoulos, Alexandros
- ORCID
- Babaei, Rohollah
- Schuster, Maximilian
- Meln, Irina
- Ghandour, Rayane A.
- Pisani, Didier F.
- Wu, Shuang
- Schoiswohl, Gabriele
- Billeter, Adrian T.
- Krunic, Damir
- Mauer, Jan
- Lee, Yun-Hee
- Granneman, James G.
- Fischer, Lars
- Müller-Stich, Beat P.
- Amri, Ez-Zoubir
- Kershaw, Erin E.
- Heikenwälder, Mathias
- Herzig, Stephan
- Vegiopoulos, Alexandros
- Venue
- Science Signaling
- Published
- 2018-04-24
- Volume
- 11
- Issue
- 527
- Pages
- eaai7838
- ISSN
- 1937-9145 (ISSN-L)
- 1945-0877
- OpenAlex
- W2801208163
- Cited by
- 53
- References
- 5
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 10 · 2023: 6 · 2022: 5 · 2021: 8 · 2020: 10 · 2019: 9 · 2018: 2
- FWCI
- 4.99
- Type
- journal article
- Language
- en
- Open access
- Locations
- Science Signaling (publishedVersion)
- PubMed (publishedVersion)
- Site cant be reached (submittedVersion)
- HAL (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- PuSH - Publication Server of Helmholtz Zentrum München (submittedVersion)
- Funders
- National Institutes of Health (R01DK090166)
- Human Frontier Science Program (RGY0082/2014)
- Deutsche Forschungsgemeinschaft (HE 3260/8-1)
- China Scholarship Council
- Topics
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- beige adipogenesis, adipose tissue inflammation, adipose tissue remodeling, adipocyte lipolysis, adipose triglyceride lipase, IL-6 family cytokines, beta3-adrenergic receptor, adipocyte progenitors, stromal cells
- MeSH terms
- Adipocytes, Beige, Acyltransferases, Adipose Tissue, Animals, Cell Differentiation, Cells, Cultured, Female, Humans, Inflammation, Lipase, Mice, Inbred C57BL, Signal Transduction, Transforming Growth Factor beta, Mice, Knockout, Gene Expression Profiling, Adipogenesis, STAT3 Transcription Factor, Janus Kinases
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