ArticleNature medicine2011
Uncoupling the mechanisms of obesity and hypertension by targeting hypothalamic IKK-β and NF-κB.
Article in Nature medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers, 1 of them a synthesis that pooled it.
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136 citing papers in PubMed, 1 synthesis or guideline pooled it, 216 citations in OpenAlex.
- Association between ambient air pollution and diabetes mellitus in Europe and North America: systematic review and meta-analysis.Environmental health perspectives · 2015Pooled it
- The NF-κB Signalling Pathway: Mechanisms, Consequences and Therapeutic Targets.Journal of cellular and molecular medicine · 2026Review
- Association between the Metabolic Score for Visceral Fat (METS-VF) and incident hypertension in middle-aged and older Chinese adults: a nationwide prospective cohort study.BMC public health · 2026Article
- Neuroendocrine-immune perturbations in metabolic disease: pathophysiological mechanisms underlying cognitive impairment.Frontiers in human neuroscience · 2026Review
- Central nervous system mechanisms of salt-sensitive hypertension.Physiological reviews · 2025Review
- Analysis of the Aerial Parts ofFood science & nutrition · 2025Article
- Hypothalamic Gliosis Is Associated With Multiple Cardiovascular Disease Risk Factors in the Framingham Heart Study.Journal of the American Heart Association · 2025Article
- Obesity- and High-Fat-Diet-Induced Neuroinflammation: Implications for Autonomic Nervous System Dysfunction and Endothelial Disorders.International journal of molecular sciences · 2025Review
- Update on Hypothalamic Inflammation and Gliosis: Expanding Evidence of Relevance Beyond Obesity.Current obesity reports · 2025Review
- The immunology of sickness metabolism.Cellular & molecular immunology · 2024Review
- Hypothalamic MRI-derived microstructure is associated with neurocognitive aging in humans.Neurobiology of aging · 2024Article
- Childhood Obesity, Hypothalamic Inflammation, and the Onset of Puberty: A Narrative Review.Nutrients · 2024Review
- [Activation ofNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- NF-κB in biology and targeted therapy: new insights and translational implications.Signal transduction and targeted therapy · 2024Review
- Maternal Western diet programs cardiometabolic dysfunction and hypothalamic inflammation via epigenetic mechanisms predominantly in the male offspring.Molecular metabolism · 2024Article
- Relationship between exposure to fine particulate matter and cardiovascular risk factors and the modifying effect of socioeconomic status: a cross-sectional study in Beijing, China.Frontiers in public health · 2024Article
- AAV-BDNF gene therapy ameliorates a hypothalamic neuroinflammatory signature in theMolecular therapy. Methods & clinical development · 2023Article
- Modulation of GABA by sodium butyrate ameliorates hypothalamic inflammation in experimental model of PCOS.BMC neuroscience · 2023Article
- Contrasting effects of sleep fragmentation and angiotensin-II treatment upon pro-inflammatory responses of mice.Scientific reports · 2022Article
- Hypothalamic inflammation in metabolic disorders and aging.Cellular and molecular life sciences : CMLS · 2021Review
76 more citing papers are in PubMed but not listed here.
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3 authors at 1 institution in 1 country.
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Abstract
Obesity-related hypertension has become an epidemic health problem and a major risk factor for the development of cardiovascular disease (CVD). Recent research on the pathophysiology of obesity has implicated a role for the hypothalamus in the pathogenesis of this condition. However, it remains unknown whether the often-seen coupling of hypertension with obesity can also be explained by hypothalamic dysfunction, despite the emerging appreciation that many forms of hypertension are neurogenic in origin. Our studies here revealed that acute activation of the proinflammatory protein nuclear factor κB (NF-κB) and its upstream activator IκB kinase-β (IKK-β, encoded by Ikbkb) in the mediobasal hypothalamus rapidly elevated blood pressure in mice independently of obesity. This form of hypothalamic inflammation-induced hypertension involved the sympathetic upregulation of hemodynamics and was reversed by sympathetic suppression. Loss-of-function studies further showed that NF-κB inhibition in the mediobasal hypothalamus counteracted obesity-related hypertension in a manner that was dissociable from changes in body weight. In addition, we found that pro-opiomelanocortin (POMC) neurons were crucial for the hypertensive effects of the activation of hypothalamic IKK-β and NF-κB, which underlie obesity-related hypertension. In conclusion, obesity-associated activation of IKK-β and NF-κB in the mediobasal hypothalamus--particularly in the hypothalamic POMC neurons--is a primary pathogenic link between obesity and hypertension. Breaking this pathogenic link may represent an avenue for controlling obesity-related hypertension and CVD without requiring obesity control.
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