ArticleProceedings of the National Academy of Sciences of the United States of America2022
An immune-sympathetic neuron communication axis guides adipose tissue browning in cancer-associated cachexia.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 68 citations in OpenAlex.
- Heterogeneity in cancer: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Unveiling the mechanism of Baoyuan Jiedu Decoction in cancer cachexia-induced lipolysis through network pharmacology and bioinformatics.Journal of traditional and complementary medicine · 2026Article
- Pancreatic cancer cachexia promotes cardiac dysfunction through altered adrenergic signalling in the heart.The Journal of physiology · 2026Article
- Glycyrrhetinic acid augments lipid catabolism via immune-neural modulation in adipose tissue.Journal of advanced research · 2026Article
- Otopetrin 1 protects against adipose tissue wasting during cancer cachexia progression.iScience · 2026Article
- Fueling or Fighting Cancer? The Thermogenic Paradox of Brown Adipose Tissue.Current obesity reports · 2026Review
- Cancer cachexia: molecular basis and therapeutic advances.Signal transduction and targeted therapy · 2026Review
- Cancer cachexia as an immunometabolic syndrome: targeting the immunometabolic interface with traditional Chinese Medicine monomers and formulas.Frontiers in immunology · 2026Review
- From endocrine to immune: therapeutic potential of brown adipose tissue in remodelling the cardiovascular immune microenvironment.Frontiers in immunology · 2026Review
- Physical Activity, Exerkines, and Their Role in Cancer Cachexia.International journal of molecular sciences · 2025Review
- Brown adipose tissue machine learning nnU-Net V2 network using TriDFusion (3DF).EJNMMI research · 2025Article
- The Influence of the Sympathetic Nervous System on Cardiometabolic Health in Response to Weight Gain or Weight Loss.Metabolites · 2025Review
- TRIM22 governs tumorigenesis and protects against endometrial cancer-associated cachexia by inhibiting inflammatory response and adipose thermogenic activity.Cancer & metabolism · 2025Article
- Clearing the path for whole-mount labeling and quantification of neuron and vessel density in adipose tissue.Journal of cell science · 2025Article
- SIRT6 Ameliorates Cancer Cachexia-Associated Adipose Wasting by Suppressing TNFR2 Signalling in Mice.Journal of cachexia, sarcopenia and muscle · 2025Article
- Brown adipose tissue is associated with reduced weight loss and risk of cancer cachexia: A retrospective cohort study.Clinical nutrition (Edinburgh, Scotland) · 2025Article
- Nerves at Play: The Peripheral Nervous System in Extracranial Malignancies.Cancer discovery · 2025Review
- Crosstalk Between the Nervous System and Colorectal Cancer.Neuroscience bulletin · 2025Review
- Imaging Brown Adipose Tissue: Current State and Future Perspective.Theranostics · 2025Review
- Crosstalk between fat tissue and muscle, brain, liver, and heart in obesity: cellular and molecular perspectives.European journal of medical research · 2024Review
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 2 countries.
Funding
Abstract
Cancer-associated cachexia (CAC) is a hypermetabolic syndrome characterized by unintended weight loss due to the atrophy of adipose tissue and skeletal muscle. A phenotypic switch from white to beige adipocytes, a phenomenon called browning, accelerates CAC by increasing the dissipation of energy as heat. Addressing the mechanisms of white adipose tissue (WAT) browning in CAC, we now show that cachexigenic tumors activate type 2 immunity in cachectic WAT, generating a neuroprotective environment that increases peripheral sympathetic activity. Increased sympathetic activation, in turn, results in increased neuronal catecholamine synthesis and secretion, β-adrenergic activation of adipocytes, and induction of WAT browning. Two genetic mouse models validated this progression of events. 1) Interleukin-4 receptor deficiency impeded the alternative activation of macrophages, reduced sympathetic activity, and restrained WAT browning, and 2) reduced catecholamine synthesis in peripheral dopamine β-hydroxylase (DBH)-deficient mice prevented cancer-induced WAT browning and adipose atrophy. Targeting the intraadipose macrophage-sympathetic neuron cross-talk represents a promising therapeutic approach to ameliorate cachexia in cancer patients.
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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.