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: 4 complete abstracts (664 words), 10 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
Members of the class of neutral glycosphingolipids. They are the basic units of sphingolipids. They are sphingoids attached via their amino groups to a long chain fatty acyl group. They abnormally accumulate in fabry disease.
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: Ceramide.
Where it fits in the MeSH classification
- Broader topics
- Amides; Neutral Glycosphingolipids
- Narrower topics
- Cerebrosides; Globosides; Lactosylceramides; Trihexosylceramides
- See also
- Fabry Disease
Related concepts
Research landscape
PubMed indexes 16,146 records tagged with the MeSH heading “Ceramides” (counts retrieved 2026-10-31). 2,583 of them (16.0%) were published from 2020 onward, and the busiest period so far is through 1999 with 5,151 records.
Reviews account for 1,600 records (9.9%) and meta-analyses for 13. Randomized controlled trials number 124 (0.8%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 5,151 |
| 2000-2009 | 4,095 |
| 2010-2019 | 4,317 |
| 2020 onward | 2,583 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,600 | 9.9% |
| Meta-analyses | 13 | 0.1% |
| Randomized controlled trials | 124 | 0.8% |
Method: PubMed query "Ceramides"[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 |
|---|---|---|---|---|
| Lipidomic profiling of human serum enables detection of pancreatic cancer | 2022 | Research article Design not recorded in structured metadata | 137 | cc by PMID 35013261 · DOI · PMC8748654 |
| Ceramides as Mediators of Oxidative Stress and Inflammation in Cardiometabolic Disease | 2022 | Review article Design not recorded in structured metadata | 90 | cc by PMID 35269861 · DOI · PMC8911014 |
| Ceramide accumulation induces mitophagy and impairs β-oxidation in PINK1 deficiency | 2021 | Research article Design not recorded in structured metadata | 80 | cc by PMID 34686591 · DOI · PMC8639384 |
| Inhibition of ceramide synthesis ameliorates body wasting in a cancer cachexia model | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42138073 · DOI · PMC13178653 |
Lipidomic profiling of human serum enables detection of pancreatic cancer [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Pancreatic cancer has the worst prognosis among all cancers.
- Closing excerpt
- Furthermore, selected lipid species indicate a potential as prognostic biomarkers.
- 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 (155 words)
Pancreatic cancer has the worst prognosis among all cancers. Cancer screening of body fluids may improve the survival time prognosis of patients, who are often diagnosed too late at an incurable stage. Several studies report the dysregulation of lipid metabolism in tumor cells, suggesting that changes in the blood lipidome may accompany tumor growth. Here we show that the comprehensive mass spectrometric determination of a wide range of serum lipids reveals statistically significant differences between pancreatic cancer patients and healthy controls, as visualized by multivariate data analysis. Three phases of biomarker discovery research (discovery, qualification, and verification) are applied for 830 samples in total, which shows the dysregulation of some very long chain sphingomyelins, ceramides, and (lyso)phosphatidylcholines. The sensitivity and specificity to diagnose pancreatic cancer are over 90%, which outperforms CA 19-9, especially at an early stage, and is comparable to established diagnostic imaging methods. Furthermore, selected lipid species indicate a potential as prognostic biomarkers.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35013261 · DOI · PMC8748654
Ceramides as Mediators of Oxidative Stress and Inflammation in Cardiometabolic Disease [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Ceramides, composed of a sphingosine and a fatty acid, are bioactive lipid molecules involved in many key cellular pathways (e.
- Closing excerpt
- This review reports available evidence on ceramide structure and generation, and discusses their role in cardiometabolic disease, as well as current translational chances and difficulties for ceramide application in the cardiometabolic clinical settings.
- 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 (88 words)
Ceramides, composed of a sphingosine and a fatty acid, are bioactive lipid molecules involved in many key cellular pathways (e.g., apoptosis, oxidative stress and inflammation). There is much evidence on the relationship between ceramide species and cardiometabolic disease, especially in relationship with the onset and development of diabetes and acute and chronic coronary artery disease. This review reports available evidence on ceramide structure and generation, and discusses their role in cardiometabolic disease, as well as current translational chances and difficulties for ceramide application in the cardiometabolic clinical settings.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35269861 · DOI · PMC8911014
Ceramide accumulation induces mitophagy and impairs β-oxidation in PINK1 deficiency [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Energy production via the mitochondrial electron transport chain (ETC) and mitophagy are two important processes affected in Parkinson's disease (PD).
- Closing excerpt
- Furthermore, our data nominate β-oxidation and ceramide as therapeutic targets for PD.
- 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 (242 words)
Energy production via the mitochondrial electron transport chain (ETC) and mitophagy are two important processes affected in Parkinson's disease (PD). Interestingly, PINK1, mutations of which cause early-onset PD, plays a key role in both processes, suggesting that these two mechanisms are connected. However, the converging link of both pathways currently remains enigmatic. Recent findings demonstrated that lipid aggregation, along with defective mitochondria, is present in postmortem brains of PD patients. In addition, an increasing body of evidence shows that sphingolipids, including ceramide, are altered in PD, supporting the importance of lipids in the pathophysiology of PD. Here, we identified ceramide to play a crucial role in PINK1-related PD that was previously linked almost exclusively to mitochondrial dysfunction. We found ceramide to accumulate in mitochondria and to negatively affect mitochondrial function, most notably the ETC. Lowering ceramide levels improved mitochondrial phenotypes in pink1-mutant flies and PINK1-deficient patient-derived fibroblasts, showing that the effects of ceramide are evolutionarily conserved. In addition, ceramide accumulation provoked ceramide-induced mitophagy upon PINK1 deficiency. As a result of the ceramide accumulation, β-oxidation in PINK1 mutants was decreased, which was rescued by lowering ceramide levels. Furthermore, stimulation of β-oxidation was sufficient to rescue PINK1-deficient phenotypes. In conclusion, we discovered a cellular mechanism resulting from PD-causing loss of PINK1 and found a protective role of β-oxidation in ETC dysfunction, thus linking lipids and mitochondria in the pathophysiology of PINK1-related PD. Furthermore, our data nominate β-oxidation and ceramide as therapeutic targets for PD.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34686591 · DOI · PMC8639384
Inhibition of ceramide synthesis ameliorates body wasting in a cancer cachexia model [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Cachexia is a metabolic wasting syndrome affecting many patients with cancer, with poor survival outcomes.
- Closing excerpt
- Our data place ceramides as contributors to metabolic dysfunction in cachexia and highlight the suitability of the ceramide synthesis pathway for therapeutic targeting.
- 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 (179 words)
Cachexia is a metabolic wasting syndrome affecting many patients with cancer, with poor survival outcomes. Disturbed lipid metabolism is a hallmark of cachexia, and our previous work has identified increased levels of circulating ceramides, which are bioactive lipids with adverse effects in metabolic diseases, as biomarkers for cachexia in mouse models and patients. Here, we investigated the role of ceramides on cachexia development using the well-established C26 colon carcinoma model. We demonstrated that elevated ceramides in cachexia arose from increased liver synthesis. We showed that ceramides directly contributed to impaired mitochondrial function and energy homeostasis in cachexia target tissues. Targeting ceramide synthesis using miRNA interference, or myriocin, an approved compound targeting the key synthesis enzyme serine palmitoyltransferase (SPT), improved markers of muscle atrophy in cachectic male mice. Importantly, we demonstrated that key enzymes involved in ceramide production were also elevated in livers, but not in other organs, of patients with cancer cachexia, correlating with disease severity. Our data place ceramides as contributors to metabolic dysfunction in cachexia and highlight the suitability of the ceramide synthesis pathway for therapeutic targeting.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42138073 · DOI · PMC13178653
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 Many ceramides [5]
- Research article When do Lasses (longevity assurance genes) become CerS (ceramide synthases)?: Insights into the regulation of ceramide synthesis [6]
- Research article Ceramides and other sphingolipids as drivers of cardiovascular disease [7]
- Research article Sphingosine 1-phosphate and ceramide 1-phosphate: expanding roles in cell signaling [8]
- Research article Roles of Diacylglycerols and Ceramides in Hepatic Insulin Resistance [9]
- Research article Lipotoxicity in nonalcoholic fatty liver disease: not all lipids are created equal [10]
References
- Wolrab D, Jirásko R, Cífková E, Höring M, Mei D, Chocholoušková M, et al.. Lipidomic profiling of human serum enables detection of pancreatic cancer. . 2022. PMID 35013261 · DOI · PMC8748654
- Gaggini M, Ndreu R, Michelucci E, Rocchiccioli S, Vassalle C. Ceramides as Mediators of Oxidative Stress and Inflammation in Cardiometabolic Disease. . 2022. PMID 35269861 · DOI · PMC8911014
- Vos M, Dulovic-Mahlow M, Mandik F, Frese L, Kanana Y, Haissatou Diaw S, et al.. Ceramide accumulation induces mitophagy and impairs β-oxidation in PINK1 deficiency. . 2021. PMID 34686591 · DOI · PMC8639384
- Morigny P, Ji H, Cussonneau L, Zorzato S, Kwon Y, Riols F, et al.. Inhibition of ceramide synthesis ameliorates body wasting in a cancer cachexia model. . 2026. PMID 42138073 · DOI · PMC13178653
- Hannun YA, Obeid LM. Many ceramides. J Biol Chem. 2011. PMID 21693702 · DOI · PMC3151029
- Pewzner-Jung Y, Ben-Dor S, Futerman AH. When do Lasses (longevity assurance genes) become CerS (ceramide synthases)?: Insights into the regulation of ceramide synthesis. J Biol Chem. 2006. PMID 16793762 · DOI
- Choi RH, Tatum SM, Symons JD, Summers SA, Holland WL. Ceramides and other sphingolipids as drivers of cardiovascular disease. Nat Rev Cardiol. 2021. PMID 33772258 · DOI · PMC8978615
- Chalfant CE, Spiegel S. Sphingosine 1-phosphate and ceramide 1-phosphate: expanding roles in cell signaling. J Cell Sci. 2005. PMID 16219683 · DOI
- Petersen MC, Shulman GI. Roles of Diacylglycerols and Ceramides in Hepatic Insulin Resistance. Trends Pharmacol Sci. 2017. PMID 28551355 · DOI · PMC5499157
- Alkhouri N, Dixon LJ, Feldstein AE. Lipotoxicity in nonalcoholic fatty liver disease: not all lipids are created equal. Expert Rev Gastroenterol Hepatol. 2009. PMID 19673631 · DOI · PMC2775708
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.