Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (695 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A group of corticosteroids that affect carbohydrate metabolism (gluconeogenesis, liver glycogen deposition, elevation of blood sugar), inhibit adrenocorticotropic hormone secretion, and possess pronounced anti-inflammatory activity. They also play a role in fat and protein metabolism, maintenance of arterial blood pressure, alteration of the connective tissue response to injury, reduction in the number of circulating lymphocytes, and functioning of the central nervous system.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Glucocorticoid; Glucocorticoid Effect; Effect, Glucocorticoid; Glucorticoid Effects; Effects, Glucorticoid.
Where it fits in the MeSH classification
- Broader topics
- Adrenal Cortex Hormones; Hormones
- See also
- Receptors, Glucocorticoid
Related concepts
- Corticosteroids
- Gluconeogenesis
- Blood Sugar
- Adrenocorticotropic Hormone
Research landscape
PubMed indexes 76,534 records tagged with the MeSH heading “Glucocorticoids” (counts retrieved 2026-10-29). 12,647 of them (16.5%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 24,084 records.
Reviews account for 14,147 records (18.5%) and meta-analyses for 943. Randomized controlled trials number 4,513 (5.9%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 19,701 |
| 2000-2009 | 20,102 |
| 2010-2019 | 24,084 |
| 2020 onward | 12,647 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 14,147 | 18.5% |
| Meta-analyses | 943 | 1.2% |
| Randomized controlled trials | 4,513 | 5.9% |
Method: PubMed query "Glucocorticoids"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in pharmacology
Drug evidence builds in layers: laboratory pharmacology describes how a compound acts, pharmacokinetic studies describe how the body handles it, and randomized trials test whether it helps and what harms it causes. Post-marketing surveillance and observational studies reveal rarer adverse effects but cannot prove causation. This page is educational and is not a recommendation to start, stop or change any medicine; decisions about treatment belong with a qualified clinician.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Chronic Restraint Stress Misaligns Corneal Clock via β-Adrenergic and Glucocorticoid Signaling, Altering Epithelial, Neural, Immune, Metabolic States | 2025 | Research article Design not recorded in structured metadata | 5 | cc by PMID 41400316 · DOI · PMC12720190 |
| Mortality risk and causes of death in exogenous Cushing's syndrome: a systematic review and meta-analysis | 2026 | Meta-analysis Design not recorded in structured metadata | 3 | cc by PMID 41873700 · DOI · PMC13183439 |
| Quantitative proteomics and phosphoproteomics reveal glucocorticoid stimulation of TLR and Rho GTPase signaling in neutrophil-like cells | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 41645235 · DOI · PMC12964602 |
Chronic Restraint Stress Misaligns Corneal Clock via β-Adrenergic and Glucocorticoid Signaling, Altering Epithelial, Neural, Immune, Metabolic States [1]
Abstract reading summary — source excerpts
- Opening excerpt
- PurposeTo determine whether chronic restraint stress (RS), a validated model of chronic psychological stress, disrupts the corneal circadian transcriptome and alters epithelial, neural, immune, and metabolic outputs, and to distinguish the relative contributions of β-adrenergic and glucocorticoid signaling.
- Closing excerpt
- Temporal targeting of these neuroendocrine pathways may represent a strategy to mitigate stress-induced ocular-surface dysfunction.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (237 words)
PurposeTo determine whether chronic restraint stress (RS), a validated model of chronic psychological stress, disrupts the corneal circadian transcriptome and alters epithelial, neural, immune, and metabolic outputs, and to distinguish the relative contributions of β-adrenergic and glucocorticoid signaling.MethodsMale C57BL/6J mice were subjected to RS for 2 h/day at ZT3 (Zeitgeber Time 3) for 14 consecutive days. Cohorts received either propranolol, metyrapone, or no intervention; non-stressed littermates served as controls. Systemic stress activation was confirmed via plasma levels of adrenocorticotropic hormone, corticosterone, epinephrine, and norepinephrine, along with superior cervical ganglion and adrenal gene expression. Whole corneas were collected every three hours over a 24-hour cycle (ZT0-ZT21) and analyzed by bulk RNA sequencing. Rhythmic transcripts were identified using JTK_CYCLE; differential gene screening was performed using DESeq2. Epithelial mitoses, immune-cell counts, ZO-1/occludin expression, subbasal nerve architecture, and Cochet-Bonnet corneal sensitivity were assessed.ResultsRS induced a broad phase advance and amplitude attenuation of rhythmic genes, with downstream reprogramming of immune, proliferative, and metabolic pathways. Phenotypically, RS increased corneal mechanical sensitivity, reduced neutrophil and γδ T-cell counts, elevated epithelial mitotic activity, and diminished ZO-1/occludin expression, whereas subbasal nerve length remained unaffected. Propranolol partially restored circadian phase alignment and improved epithelial and metabolic parameters; metyrapone preferentially enhanced immune-related gene activity and immune-cell abundance.ConclusionsRS disrupts corneal circadian output and impairs epithelial, immune, and metabolic homeostasis via β-adrenergic and glucocorticoid mechanisms. Temporal targeting of these neuroendocrine pathways may represent a strategy to mitigate stress-induced ocular-surface dysfunction.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41400316 · DOI · PMC12720190
Mortality risk and causes of death in exogenous Cushing's syndrome: a systematic review and meta-analysis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- ContextChronic oral glucocorticoids (GCs) are widely prescribed for multiple diseases.
- Closing excerpt
- These findings support GC stewardship and targeted cardiovascular and infection risk mitigation, rather than indiscriminate dose reduction.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (253 words)
ContextChronic oral glucocorticoids (GCs) are widely prescribed for multiple diseases. Although long-term GC exposure causes systemic toxicity, the magnitude, dose-response relationship, and causes of GC-associated mortality remain incompletely defined.ObjectiveTo quantify overall and cause-specific mortality associated with chronic oral GC exposure and evaluate dose-response relationships across underlying disease groups.MethodsWe conducted a systematic review and meta-analysis following PRISMA guidelines (PROSPERO CRD42017067530). PubMed/MEDLINE, EMBASE, Cochrane Library, Web of Science, and CINAHL were searched from 1945 to March 2019. Eligible studies reported standardized mortality ratios (SMRs) or absolute deaths among adults receiving chronic oral GCs. Random-effects meta-analysis and mixed-effects meta-regression were used to synthesize mortality and dose-response associations across GC exposure metrics, exposure duration, and disease subgroups.ResultsOne-hundred and sixteen studies encompassing 128 cohorts and 51 380 patients were included. Chronic GC exposure was associated with excess mortality (pooled SMR 1.87; 95%CI 1.32-2.61; I2 74.0%). The pooled proportion of death was 12.0% (95%CI 10-14%). Mortality risk was highest in inflammatory diseases (30.0%) and the vasculitides (18.0%). Higher cumulative dose (≥5 g prednisolone-equivalent), average daily dose >5 mg/day, and higher initial dose were each independently associated with increased mortality. Cardiovascular disease was the leading causes of death (25.6%), followed by malignancy (15.7%) and infection (13.4%).ConclusionChronic oral GC exposure was associated with increased mortality across disease groups, with higher cumulative and early-treatment doses correlating with higher risk. However, causal attribution remains uncertain due to confounding by indication, limited disease-severity data, and exposure misclassification. These findings support GC stewardship and targeted cardiovascular and infection risk mitigation, rather than indiscriminate dose reduction.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41873700 · DOI · PMC13183439
Quantitative proteomics and phosphoproteomics reveal glucocorticoid stimulation of TLR and Rho GTPase signaling in neutrophil-like cells [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundGlucocorticoids are corticosteroid hormones that are commonly used for treating systemic inflammatory diseases and acute infections.
- Closing excerpt
- ConclusionsOur results not only reveal unconventional regulatory mechanisms of glucocorticoids in the human immune system but also provide valuable resources for discovering novel glucocorticoid-responsive protein targets in neutrophils.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (205 words)
BackgroundGlucocorticoids are corticosteroid hormones that are commonly used for treating systemic inflammatory diseases and acute infections. Immunosuppressive effects of glucocorticoids have been studied in many cell types, particularly macrophages and T cells. Despite the importance and abundance of neutrophils in the human immune system, glucocorticoid responses remain understudied in neutrophils.ResultsHere, we perform quantitative mass spectrometry-based proteomics of primary neutrophils and neutrophil-like cells differentiated from human HL-60 promyelocyte cells. Primary neutrophils exhibited CK2 kinase activation and increase phosphorylation of HSP90 following 2-h incubation, highlighting potential effects of short-term ex vivo handling. Proteome and flow cytometry analysis show that neutrophil-like cells share features of neutrophils. Quantitative proteomics and phosphoproteomics of neutrophil-like cells treated with two synthetic glucocorticoid compounds, the clinical drugs dexamethasone and prednisolone, identify higher numbers of significantly regulated proteins and phosphosites compared to parental HL-60 cells. Glucocorticoid treatments modulated toll-like receptor signaling and CXCR4 serine phosphorylation. In addition, we identify RIPOR2 as a glucocorticoid-regulated protein associated with Rho GTPase signaling networks and actin cytoskeletal remodeling in neutrophils and neutrophil-like cells, though its exact functional role requires further investigation.ConclusionsOur results not only reveal unconventional regulatory mechanisms of glucocorticoids in the human immune system but also provide valuable resources for discovering novel glucocorticoid-responsive protein targets in neutrophils.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41645235 · DOI · PMC12964602
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Comparison of Pharmaceutical, Psychological, and Exercise Treatments for Cancer-Related Fatigue: A Meta-analysis [4]
- Research article Anaphylaxis-a 2020 practice parameter update, systematic review, and Grading of Recommendations, Assessment, Development and Evaluation (GRADE) analysis [5]
- Research article A meta-analysis of glucocorticoids as modulators of oxidative stress in vertebrates [6]
- Research article Corticosteroids for the treatment of Duchenne muscular dystrophy [7]
- Research article Contemporary management of chronic obstructive pulmonary disease: scientific review [8]
- Research article Glucocorticosteroid therapy in inflammatory bowel disease: systematic review and meta-analysis [9]
References
- Xuan S, Yang T, Ba M, Zhang W, Yang J, Pei X, et al.. Chronic Restraint Stress Misaligns Corneal Clock via β-Adrenergic and Glucocorticoid Signaling, Altering Epithelial, Neural, Immune, Metabolic States. . 2025. PMID 41400316 · DOI · PMC12720190
- Limumpornpetch P, Stewart PM, Pujades-Rodriguez M, Baxter PD, Tiganescu A, Nyaga VN, et al.. Mortality risk and causes of death in exogenous Cushing's syndrome: a systematic review and meta-analysis. . 2026. PMID 41873700 · DOI · PMC13183439
- Cho H, Nielsen ML, Olsen JV. Quantitative proteomics and phosphoproteomics reveal glucocorticoid stimulation of TLR and Rho GTPase signaling in neutrophil-like cells. . 2026. PMID 41645235 · DOI · PMC12964602
- Mustian KM, Alfano CM, Heckler C, Kleckner AS, Kleckner IR, Leach CR, et al.. Comparison of Pharmaceutical, Psychological, and Exercise Treatments for Cancer-Related Fatigue: A Meta-analysis. JAMA Oncol. 2017. PMID 28253393 · DOI · PMC5557289
- Shaker MS, Wallace DV, Golden DBK, Oppenheimer J, Bernstein JA, Campbell RL, et al.. Anaphylaxis-a 2020 practice parameter update, systematic review, and Grading of Recommendations, Assessment, Development and Evaluation (GRADE) analysis. J Allergy Clin Immunol. 2020. PMID 32001253 · DOI
- Costantini D, Marasco V, Møller AP. A meta-analysis of glucocorticoids as modulators of oxidative stress in vertebrates. J Comp Physiol B. 2011. PMID 21416253 · DOI
- Matthews E, Brassington R, Kuntzer T, Jichi F, Manzur AY. Corticosteroids for the treatment of Duchenne muscular dystrophy. Cochrane Database Syst Rev. 2016. PMID 27149418 · DOI · PMC8580515
- Sin DD, McAlister FA, Man SF, Anthonisen NR. Contemporary management of chronic obstructive pulmonary disease: scientific review. JAMA. 2003. PMID 14600189 · DOI
- Ford AC, Bernstein CN, Khan KJ, Abreu MT, Marshall JK, Talley NJ, et al.. Glucocorticosteroid therapy in inflammatory bowel disease: systematic review and meta-analysis. Am J Gastroenterol. 2011. PMID 21407179 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.