ReviewCurrent atherosclerosis reports2013
Modulation of 11β-hydroxysteroid dehydrogenase as a strategy to reduce vascular inflammation.
Review in Current atherosclerosis reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 38 citations in OpenAlex.
- Prednisolone-containing liposomes accumulate in human atherosclerotic macrophages upon intravenous administration.Nanomedicine : nanotechnology, biology, and medicine · 2015Trial
- Multi-omics profiling reveals molecular features of visceral adiposity in autonomous cortisol secretion.iScience · 2026Article
- Single-Cell Analysis Uncovers Osteoblast Factor Growth Differentiation Factor 10 as Mediator of Vascular Smooth Muscle Cell Phenotypic Modulation Associated with Plaque Rupture in Human Carotid Artery Disease.International journal of molecular sciences · 2022Article
- Glucocorticoids: Fuelling the Fire of Atherosclerosis or Therapeutic Extinguishers?International journal of molecular sciences · 2021Review
- 11β-hydroxysteroid dehydrogenases: A growing multi-tasking family.Molecular and cellular endocrinology · 2021Review
- Metformin activated AMPK signaling contributes to the alleviation of LPS-induced inflammatory responses in bovine mammary epithelial cells.BMC veterinary research · 2021Article
- Enhanced Angiogenesis by 11βHSD1 Blockage Is Insufficient to Improve Reperfusion Following Hindlimb Ischaemia.Frontiers in cardiovascular medicine · 2021Article
- High-fat diet and chronic stress aggravate adrenal function abnormality induced by prenatal caffeine exposure in male offspring rats.Scientific reports · 2017Article
- Virtual screening applications in short-chain dehydrogenase/reductase research.The Journal of steroid biochemistry and molecular biology · 2017Review
- Getting to the heart of intracellular glucocorticoid regeneration: 11β-HSD1 in the myocardium.Journal of molecular endocrinology · 2017Review
- A novel role for the mineralocorticoid receptor in glucocorticoid driven vascular calcification.Vascular pharmacology · 2016Article
- Article
- Review
- The multifaceted mineralocorticoid receptor.Comprehensive Physiology · 2014Review
- Expression of mineralocorticoid and glucocorticoid receptors in preautonomic neurons of the rat paraventricular nucleus.American journal of physiology. Regulatory, integrative and comparative physiology · 2014Article
- Blood pressure and amiloride-sensitive sodium channels in vascular and renal cells.Nature reviews. Nephrology · 2014Review
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Atherosclerosis is a chronic inflammatory disease in which initial vascular damage leads to extensive macrophage and lymphocyte infiltration. Although acutely glucocorticoids suppress inflammation, chronic glucocorticoid excess worsens atherosclerosis, possibly by exacerbating systemic cardiovascular risk factors. However, glucocorticoid action within the lesion may reduce neointimal proliferation and inflammation. Glucocorticoid levels within cells do not necessarily reflect circulating levels due to pre-receptor metabolism by 11β-hydroxysteroid dehydrogenases (11β-HSDs). 11β-HSD2 converts active glucocorticoids into inert 11-keto forms. 11β-HSD1 catalyses the reverse reaction, regenerating active glucocorticoids. 11β-HSD2-deficiency/inhibition causes hypertension, whereas deficiency/inhibition of 11β-HSD1 generates a cardioprotective lipid profile and improves glycemic control. Importantly, 11β-HSD1-deficiency/inhibition is atheroprotective, whereas 11β-HSD2-deficiency accelerates atherosclerosis. These effects are largely independent of systemic risk factors, reflecting modulation of glucocorticoid action and inflammation within the vasculature. Here, we consider whether evidence linking the 11β-HSDs to vascular inflammation suggests these isozymes are potential therapeutic targets in vascular injury and atherosclerosis.
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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.