ReviewAging2012
Inflammatory cause of metabolic syndrome via brain stress and NF-κB.
Review in Aging, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 4 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
103 citing papers in PubMed, 4 syntheses or guidelines pooled it, 184 citations in OpenAlex.
- Non-alcoholic Fatty Liver Disease: Also a Disease of the Brain? A Systematic Review of the Preclinical Evidence.Neurochemical research · 2024Pooled it
- Dose-response relationship of serum ferritin and dietary iron intake with metabolic syndrome and non-alcoholic fatty liver disease incidence: a systematic review and meta-analysis.Frontiers in nutrition · 2024Pooled it
- Risk of dementia or cognitive impairment in non-alcoholic fatty liver disease: A systematic review and meta-analysis.Frontiers in aging neuroscience · 2022Pooled it
- Meditation and Cardiovascular Risk Reduction: A Scientific Statement From the American Heart Association.Journal of the American Heart Association · 2017Guideline
- Metainflammation, Mitochondrial Dysfunction, and Organokine Crosstalk: A Central Axis Linking Metabolic Syndrome to Cardiovascular Diseases.International journal of molecular sciences · 2026Review
- The role of metabolic health in neurostructural and cognitive alterations in bipolar disorders.Psychological medicine · 2026Article
- Brain senescence drives sarcopenia-like transcriptomic remodeling in skeletal muscle.GeroScience · 2026Article
- Quinone reductase 2bioRxiv : the preprint server for biology · 2026Article
- Irradiation-induced brain senescence accelerates cardiac aging via systemic mechanisms: insights from transcriptomic profiling.GeroScience · 2026Article
- Chronic Stress Disrupts Immune and Endocrine Axis, Inducing Persistent Behavioral Impairments in Male Rats: In Silico and In Vivo Insights.Neurochemical research · 2025Article
- Epigenetics of Chronic Stress: Mechanisms and Health Impacts.Current genomics · 2025Review
- A biological rhythm in the hypothalamic system links sleep-wake cycles with feeding-fasting cycles.Scientific reports · 2024Article
- MicroRNA-195-5p Inhibits Intracerebral Hemorrhage-Induced Inflammatory Response and Neuron Cell Apoptosis.International journal of molecular sciences · 2024Article
- Neuroinflammation: A Modifiable Pathway Linking Obesity, Alzheimer's disease, and Depression.The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry · 2023Review
- Polystyrene Microplastics Exacerbate Systemic Inflammation in High-Fat Diet-Induced Obesity.International journal of molecular sciences · 2023Article
- Nicotinamide Prevents Diabetic Brain Inflammation via NAD+-Dependent Deacetylation Mechanisms.Nutrients · 2023Article
- Article
- Adipose tissue, systematic inflammation, and neurodegenerative diseases.Neural regeneration research · 2023Review
- Hypothalamic volume is associated with body mass index.NeuroImage. Clinical · 2023Article
- A Novel Aryl Hydrocarbon Receptor Antagonist HBU651 Ameliorates Peripheral and Hypothalamic Inflammation in High-Fat Diet-Induced Obese Mice.International journal of molecular sciences · 2022Article
43 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic syndrome, a network of medical disorders that greatly increase the risk for developing metabolic and cardiovascular diseases, has reached epidemic levels in many areas of today's world. Despite this alarming medicare situation, scientific understandings on the root mechanisms of metabolic syndrome are still limited, and such insufficient knowledge contributes to the relative lack of effective treatments or preventions for related diseases. Recent interdisciplinary studies from neuroendocrinology and neuroimmunology fields have revealed that overnutrition can trigger intracellular stresses to cause inflammatory changes mediated by molecules that control innate immunity. This type of nutrition-related molecular inflammation in the central nervous system, particularly in the hypothalamus, can form a common pathogenic basis for the induction of various metabolic syndrome components such as obesity, insulin resistance, and hypertension. Proinflammatory NF-κB pathway has been revealed as a key molecular system for pathologic induction of brain inflammation, which translates overnutrition and resulting intracellular stresses into central neuroendocrine and neural dysregulations of energy, glucose, and cardiovascular homeostasis, collectively leading to metabolic syndrome. This article reviews recent research advances in the neural mechanisms of metabolic syndrome and related diseases from the perspective of pathogenic induction by intracellular stresses and NF-κB pathway of the brain.
Indexed as
Identifiers
What OpenQuestion holds
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.