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 (650 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
Steroids with a hydroxyl group at C-3 and most of the skeleton of cholestane. Additional carbon atoms may be present in the side chain. (iupac Steroid Nomenclature, 1987)
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: Sterol.
Where it fits in the MeSH classification
- Broader topics
- Cholestanes; Membrane Lipids
- Narrower topics
- Adosterol; Cholecalciferol; Cholesterol; Ergocalciferols; Fusidic Acid; Lanosterol; Phytosterols; Solanine
Related concepts
- Iupac
Research landscape
PubMed indexes 236,295 records tagged with the MeSH heading “Sterols” (counts retrieved 2026-10-31). 33,069 of them (14.0%) were published from 2020 onward, and the busiest period so far is through 1999 with 101,804 records.
Reviews account for 21,010 records (8.9%) and meta-analyses for 2,108. Randomized controlled trials number 12,724 (5.4%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 101,804 |
| 2000-2009 | 46,594 |
| 2010-2019 | 54,828 |
| 2020 onward | 33,069 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 21,010 | 8.9% |
| Meta-analyses | 2,108 | 0.9% |
| Randomized controlled trials | 12,724 | 5.4% |
Method: PubMed query "Sterols"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
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 |
|---|---|---|---|---|
| SARS-CoV-2 ORF3a blocks lysosomal cholesterol egress by disrupting VPS39-regulated NPC2 trafficking and BMP metabolism | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42287635 · DOI · PMC13378056 |
| Predictive value of the combined cholesterol, high-density lipoprotein, glucose and frailty indices for cardiometabolic multimorbidity incidence: evidence from a national prospective cohort study | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42144600 · DOI · PMC13348554 |
| SREBP2 promotes macrophage alternative activation and allergic airway inflammation independent of cholesterol biosynthesis | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42236481 · DOI · PMC13448065 |
SARS-CoV-2 ORF3a blocks lysosomal cholesterol egress by disrupting VPS39-regulated NPC2 trafficking and BMP metabolism [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Cholesterol homeostasis depends on lysosomes liberating cholesterol from degraded lipids.
- Closing excerpt
- These findings identify dual functions of VPS39-regulating retromer trafficking and BMP biosynthesis-and also reveal how ORF3a blocks lysosomal cholesterol egress.
- 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 (145 words)
Cholesterol homeostasis depends on lysosomes liberating cholesterol from degraded lipids. We show that SARS-CoV-2 blocks lysosomal cholesterol egress through the viral protein ORF3a. ORF3a binds the HOPS subunit VPS39 via the W193 and Y184 residues. Disrupting this interface restores cholesterol trafficking. Mechanistically, the ORF3a-VPS39 interaction exerts dual effects. First, it traps the retromer complex on endolysosomes, preventing endosome-to-Golgi recycling and mislocalizing the cholesterol transporter NPC2. Retromer deletion reproduced these defects, whereas the ORF3a W193A mutant restored retromer trafficking. Second, ORF3a-VPS39 interaction reduces bis(monoacylglycerol)phosphates (BMPs), lysosomal lipids required for cholesterol egress, by disrupting the transfer of their precursor, phosphatidylglycerols, from mitochondria. Lipidomics revealed increased mitochondrial and decreased lysosomal phosphatidylglycerol metabolites. Disturbing autophagy or mitochondrion-derived vesicles did not alter BMP levels, whereas ORF3a reduced mitochondrion-lysosome membrane contacts. These findings identify dual functions of VPS39-regulating retromer trafficking and BMP biosynthesis-and also reveal how ORF3a blocks lysosomal cholesterol egress.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42287635 · DOI · PMC13378056
Predictive value of the combined cholesterol, high-density lipoprotein, glucose and frailty indices for cardiometabolic multimorbidity incidence: evidence from a national prospective cohort study [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundThe cholesterol, high-density lipoprotein, and glucose (CHG) is a surrogate of insulin resistance, while frailty reflects cumulative physiological decline, yet their combined utility for cardiometabolic multimorbidity (CMM) is underexplored.
- Closing excerpt
- As an accessible tool integrating routine metabolic and physiologic reserve measures, CHG-FI offers a practical alternative approach for risk stratification.
- 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 (334 words)
BackgroundThe cholesterol, high-density lipoprotein, and glucose (CHG) is a surrogate of insulin resistance, while frailty reflects cumulative physiological decline, yet their combined utility for cardiometabolic multimorbidity (CMM) is underexplored. We evaluated a combined CHG-frailty index (CHG-FI) for incident heart disease, stroke, diabetes, and CMM.MethodsWe conducted a retrospective cohort study of 6812 Chinese adults aged ≥ 45 years enrolled in the 2011-2020 waves of the China Health and Retirement Longitudinal Study (CHARLS). Participants with baseline lipid and fasting glucose measurements were included and followed prospectively for incident heart disease, stroke, diabetes, and cardiometabolic multimorbidity (≥ 2 conditions). FI was calculated using the cumulative deficit approach, and CHG was incorporated according to established procedures. Multivariable Cox regression estimated associations; CHG-FI interaction was assessed on multiplicative and additive scales. Incremental predictive utility of CHG, FI, TYG‑FI, and CHG‑FI was compared using receiver operating characteristic (ROC) curves, net reclassification improvement (NRI), and decision curve analysis (DCA). Stratified and sensitivity analyses evaluated robustness.ResultsOver a median follow‑up of 9.0 years, we observed 1,304 heart disease events, 554 strokes, 932 diabetes cases, and 467 CMM cases. Each 1-unit increase in CHG-FI was associated with higher risk: heart disease (HR 1.34, 95% CI 1.23-1.45), stroke (HR 1.85, 95% CI 1.65-2.06), diabetes (HR 1.29, 95% CI 1.17-1.42), and CMM (HR 1.79, 95% CI 1.58-2.04). Associations showed dose-response patterns and nonlinearity. The multiplicative interaction between CHG and FI for CMM was 0.54 (95% CI 0.35-0.83), reflecting a "risk saturation" or ceiling effect. Despite this, the combined CHG -FI index offered superior predictive performance for CMM relative to individual components: AUC 0.652 (95% CI 0.627-0.678), with significant improvement in reclassification (NRI 0.329, 95% CI 0.236-0.423) and discrimination (IDI 0.011, 95% CI 0.008-0.015). CHG -FI and TyG -FI showed broadly comparable performance across outcomes.ConclusionThe combined CHG-frailty index was significantly associated with incident cardiometabolic multimorbidity and its individual components, demonstrating predictive performance comparable to established combined indices. As an accessible tool integrating routine metabolic and physiologic reserve measures, CHG-FI offers a practical alternative approach for risk stratification.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42144600 · DOI · PMC13348554
SREBP2 promotes macrophage alternative activation and allergic airway inflammation independent of cholesterol biosynthesis [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Immunometabolic reprogramming is increasingly recognized as a critical regulator of macrophage activation and function.
- Closing excerpt
- These findings highlight the pivotal role of the SREBP2-IRF4 axis in modulating M2 polarization of IMs and suggest potential therapeutic targets for asthma treatment.
- 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 (171 words)
Immunometabolic reprogramming is increasingly recognized as a critical regulator of macrophage activation and function. This study aimed to elucidate the role of the SREBP2-cholesterol biosynthetic pathway in M2 activation of interstitial macrophages (IMs) during allergic asthma. We observed a significant expansion of M2-polarized IMs with heightened SREBP2-cholesterol biosynthetic activity in the lungs of asthmatic mice. IL4, a key pro-allergic cytokine in allergic asthma, was found to induce SREBP2 maturation and activate the cholesterol biosynthetic signaling pathway in macrophages. Moreover, inhibiting SREBP2 maturation restrains IL4-induced M2 activation, both in vitro and in vivo. Intriguingly, this effect was independent of intracellular cholesterol levels; instead, cholesterol itself negatively regulated SREBP2 maturation and M2 activation. Mechanistically, mature SREBP2 transcriptional modulated IRF4 expression and interacted with it to promote IL4-induced M2 activation. Additionally, myeloid-specific Scap deficiency impeded the SREBP2 maturation process in macrophages, leading to reduced M2 activation and allergic airway inflammation. These findings highlight the pivotal role of the SREBP2-IRF4 axis in modulating M2 polarization of IMs and suggest potential therapeutic targets for asthma treatment.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42236481 · DOI · PMC13448065
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 Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials [4]
- Research article The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of individual data from 27 randomised trials [5]
- Research article Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study [6]
- Research article Association Between Lowering LDL-C and Cardiovascular Risk Reduction Among Different Therapeutic Interventions: A Systematic Review and Meta-analysis [7]
- Research article Efficacy and safety of LDL-lowering therapy among men and women: meta-analysis of individual data from 174,000 participants in 27 randomised trials [8]
- Research article Long-term consequences of breastfeeding on cholesterol, obesity, systolic blood pressure and type 2 diabetes: a systematic review and meta-analysis [9]
References
- Goodson BA, Montenegro Vazquez V, Doyle A, Kolaczkowski OM, Liu R, Jia J, et al.. SARS-CoV-2 ORF3a blocks lysosomal cholesterol egress by disrupting VPS39-regulated NPC2 trafficking and BMP metabolism. . 2026. PMID 42287635 · DOI · PMC13378056
- Fan H, Jiang G, Cheng J, Chen H. Predictive value of the combined cholesterol, high-density lipoprotein, glucose and frailty indices for cardiometabolic multimorbidity incidence: evidence from a national prospective cohort study. . 2026. PMID 42144600 · DOI · PMC13348554
- Wu Y, Zheng K, Dong L, Gao S, Wu Y, Liu Z, et al.. SREBP2 promotes macrophage alternative activation and allergic airway inflammation independent of cholesterol biosynthesis. . 2026. PMID 42236481 · DOI · PMC13448065
- Cholesterol Treatment Trialists’ (CTT) Collaboration, Baigent C, Blackwell L, Emberson J, Holland LE, Reith C, et al.. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. Lancet. 2010. PMID 21067804 · DOI · PMC2988224
- Cholesterol Treatment Trialists' (CTT) Collaborators, Mihaylova B, Emberson J, Blackwell L, Keech A, Simes J, et al.. The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of individual data from 27 randomised trials. Lancet. 2012. PMID 22607822 · DOI · PMC3437972
- Voight BF, Peloso GM, Orho-Melander M, Frikke-Schmidt R, Barbalic M, Jensen MK, et al.. Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study. Lancet. 2012. PMID 22607825 · DOI · PMC3419820
- Silverman MG, Ference BA, Im K, Wiviott SD, Giugliano RP, Grundy SM, et al.. Association Between Lowering LDL-C and Cardiovascular Risk Reduction Among Different Therapeutic Interventions: A Systematic Review and Meta-analysis. JAMA. 2016. PMID 27673306 · DOI
- Cholesterol Treatment Trialists' (CTT) Collaboration, Fulcher J, O'Connell R, Voysey M, Emberson J, Blackwell L, et al.. Efficacy and safety of LDL-lowering therapy among men and women: meta-analysis of individual data from 174,000 participants in 27 randomised trials. Lancet. 2015. PMID 25579834 · DOI
- Horta BL, Loret de Mola C, Victora CG. Long-term consequences of breastfeeding on cholesterol, obesity, systolic blood pressure and type 2 diabetes: a systematic review and meta-analysis. Acta Paediatr. 2015. PMID 26192560 · 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 2026-10-31.
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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.