ReviewCurrent hypertension reports2017
11β-Hydroxysteroid Dehydrogenases and Hypertension in the Metabolic Syndrome.
Review in Current hypertension reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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
21 citing papers in PubMed, 42 citations in OpenAlex.
- Sex differences in the renal T cell profile in DOCA-salt hypertension are independent of MR activation and increases in blood pressure.American journal of physiology. Renal physiology · 2026Article
- Determination of hydrocortisone and cortisone in artificial saliva by spray assisted fine droplet formation liquid phase microextraction coupled to LC-MS/MS.Scientific reports · 2026Article
- The roles, mechanisms, and therapeutic implications of glucocorticoids in glucose and lipid metabolism.Military Medical Research · 2026Review
- Should adrenal incidentaloma patients be evaluated for muscle mass, function, and quality? A cross-sectional study.Endocrine · 2025Article
- Serum Cortisol and Cardiovascular Disease Risk - A Potential Biomarker.Current cardiology reviews · 2025Review
- Downregulation of the kidney glucagon receptor, essential for renal function and systemic homeostasis, contributes to chronic kidney disease.Cell metabolism · 2024Article
- Comprehensive strategy for identifying extracellular vesicle surface proteins as biomarkers for chronic kidney disease.Frontiers in physiology · 2024Review
- Sodium - a systematic review for Nordic Nutrition Recommendations 2023.Food & nutrition research · 2024Review
- Obesity and hypertension: Obesity medicine association (OMA) clinical practice statement (CPS) 2023.Obesity pillars · 2023Article
- High salt intake activates the hypothalamic-pituitary-adrenal axis, amplifies the stress response, and alters tissue glucocorticoid exposure in mice.Cardiovascular research · 2023Article
- 11β-Hydroxysteroid Dehydrogenase Type 1 as a Potential Treatment Target in Cardiovascular Diseases.Journal of clinical medicine · 2022Review
- Programming of Vascular Dysfunction by Maternal Stress: Immune System Implications.Frontiers in physiology · 2022Review
- Phytochemicals as Potential Epidrugs in Type 2 Diabetes Mellitus.Frontiers in endocrinology · 2021Review
- Bariatric surgery for the treatment of chronic kidney disease in obesity and type 2 diabetes mellitus.Nature reviews. Nephrology · 2020Review
- Synthesis of Novel 2-(Isopropylamino)thiazol-4(5Molecules (Basel, Switzerland) · 2020Article
- Prevalence and risk factors associated with systemic hypertension in dogs with spontaneous hyperadrenocorticism.Journal of veterinary internal medicine · 2020Article
- Sodium Handling and Interaction in Numerous Organs.American journal of hypertension · 2020Review
- Type-2 11β-hydroxysteroid dehydrogenase promotes the metastasis of colorectal cancer via the Fgfbp1-AKT pathway.American journal of cancer research · 2020Article
- Molecular Mechanisms of Primary Aldosteronism.Endocrinology and metabolism (Seoul, Korea) · 2019Review
- Lack of Renal Tubular Glucocorticoid Receptor Decreases the Thiazide-Sensitive NaFrontiers in physiology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The metabolic syndrome describes a clustering of risk factors-visceral obesity, dyslipidaemia, insulin resistance, and salt-sensitive hypertension-that increases mortality related to cardiovascular disease, type 2 diabetes, cancer, and non-alcoholic fatty liver disease. The prevalence of these concurrent comorbidities is ~ 25-30% worldwide, and metabolic syndrome therefore presents a significant global public health burden. Evidence from clinical and preclinical studies indicates that glucocorticoid excess is a key causal feature of metabolic syndrome. This is not increased systemic in circulating cortisol, rather increased bioavailability of active glucocorticoids within tissues. This review examines the role of covert glucocorticoid excess on the hypertension of the metabolic syndrome. Here, the role of the 11β-hydroxysteroid dehydrogenase enzymes, which exert intracrine and paracrine control over glucocorticoid signalling, is examined. 11βHSD1 amplifies glucocorticoid action in cells and contributes to hypertension through direct and indirect effects on the kidney and vasculature. The deactivation of glucocorticoid by 11βHSD2 controls ligand access to glucocorticoid and mineralocorticoid receptors: loss of function promotes salt retention and hypertension. As for hypertension in general, high blood pressure in the metabolic syndrome reflects a complex interaction between multiple systems. The clear association between high dietary salt, glucocorticoid production, and metabolic disorders has major relevance for human health and warrants systematic evaluation.
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What Socratic 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 Socratic graph.