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 (376 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
Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides see glycerophospholipids) or sphingosine (sphingolipids). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the 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: Phosphatides; Phospholipid.
Where it fits in the MeSH classification
- Broader topics
- Membrane Lipids
- Narrower topics
- Glycerophosphates; Sphingomyelins
- See also
- Antiphospholipid Syndrome; Antibodies, Antiphospholipid
Related concepts
Research landscape
PubMed indexes 171,953 records tagged with the MeSH heading “Phospholipids” (counts retrieved 2026-10-31). 18,183 of them (10.6%) were published from 2020 onward, and the busiest period so far is through 1999 with 87,892 records.
Reviews account for 11,801 records (6.9%) and meta-analyses for 95. Randomized controlled trials number 1,447 (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 | 87,892 |
| 2000-2009 | 30,985 |
| 2010-2019 | 34,893 |
| 2020 onward | 18,183 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 11,801 | 6.9% |
| Meta-analyses | 95 | 0.1% |
| Randomized controlled trials | 1,447 | 0.8% |
Method: PubMed query "Phospholipids"[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 |
|---|---|---|---|---|
| Cardiolipin's multifaceted role in immune response: a focus on interacting proteins | 2025 | Review article Design not recorded in structured metadata | 14 | cc by PMID 41438747 · DOI · PMC12719303 |
| Aging-associated decline of phosphatidylcholine synthesis is a malleable trigger of natural mitochondrial aging | 2026 | Research article Design not recorded in structured metadata | 6 | cc by PMID 42000749 · DOI · PMC13091796 |
| Ferroptosis: The Demise of Cells Through Phospholipid Peroxidation | 2026 | Review article Design not recorded in structured metadata | 6 | cc by PMID 41858270 · DOI · PMC13104129 |
Cardiolipin's multifaceted role in immune response: a focus on interacting proteins [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Cardiolipin is a unique and essential phospholipid that plays a pivotal role in cellular function.
- Closing excerpt
- In addition, we discuss the involvement of cardiolipin in various pathological conditions in which its protein interactions contribute to immune dysregulation.
- 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 (100 words)
Cardiolipin is a unique and essential phospholipid that plays a pivotal role in cellular function. In eukaryotic cells, it is predominantly localized within the mitochondrial membranes, with the highest concentration in the inner mitochondrial membrane (IMM). Recent studies have highlighted the multifaceted role of cardiolipin in immune regulation. This review aims to provide a comprehensive overview of specific proteins that directly interact with cardiolipin and to elucidate how these interactions underlie its diverse and critical functions in innate immunity. In addition, we discuss the involvement of cardiolipin in various pathological conditions in which its protein interactions contribute to immune dysregulation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41438747 · DOI · PMC12719303
Aging-associated decline of phosphatidylcholine synthesis is a malleable trigger of natural mitochondrial aging [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Mitochondrial dysfunction is a prominent hallmark of aging contributing to the decline of metabolic plasticity in late life.
- Closing excerpt
- We thus describe a previously unrecognized natural driver of mitochondrial decline in aging that is malleable by dietary interventions.
- 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 (146 words)
Mitochondrial dysfunction is a prominent hallmark of aging contributing to the decline of metabolic plasticity in late life. While genetic distortions of mitochondrial integrity elicit premature aging, the mechanisms leading to "natural" aging of mitochondria are less clear. Here we use proteomics, lipidomics, genetics and functional tests in wild type Caenorhabditis elegans and long-lived clk-1(qm30) and isp-1(qm150) mitochondrial mutants to identify molecular pathways that support longevity amid persistent mitochondrial inefficiency. These tests and subsequent transcriptomics and metabolomics analyses in humans reveal aging-associated decline of phosphatidylcholine synthesis as a trigger of mitochondrial network disruption, which contributes to mitochondrial dysfunction during normal aging. Moreover, ectopic boosting of phosphatidylcholine levels via diet restores late life mitochondrial integrity in vivo in nematodes and reinstates metabolic resilience in human cell culture tests. We thus describe a previously unrecognized natural driver of mitochondrial decline in aging that is malleable by dietary interventions.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42000749 · DOI · PMC13091796
Ferroptosis: The Demise of Cells Through Phospholipid Peroxidation [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Ferroptosis is a form of regulated cell death driven by iron-dependent peroxidation of polyunsaturated phospholipids.
- Closing excerpt
- This review summarizes the metabolic foundations that determine the susceptibility of cells to ferroptosis and discusses the possibility of treating human diseases by modulating cellular sensitivity to ferroptosis.
- 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 (130 words)
Ferroptosis is a form of regulated cell death driven by iron-dependent peroxidation of polyunsaturated phospholipids. The susceptibility of cells to ferroptosis is often strongly shaped by lipid metabolic pathways that determine the abundance, distribution, and redox reactivity of polyunsaturated phospholipids. Enzymes that activate and incorporate polyunsaturated fatty acids into phospholipids generate the substrates whose peroxidation causes ferroptosis, thereby sensitizing cells to ferroptosis. In contrast, synthesis of monounsaturated phospholipids and the presence of lipid-soluble antioxidants limit the accumulation of phospholipid peroxides, thereby protecting cells from ferroptosis. Thus, different tissues may display characteristic ferroptotic responses caused by their unique lipid composition and antioxidant capacity. This review summarizes the metabolic foundations that determine the susceptibility of cells to ferroptosis and discusses the possibility of treating human diseases by modulating cellular sensitivity to ferroptosis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41858270 · DOI · PMC13104129
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 Phosphoinositides as membrane organizers [4]
- Research article Regulation of phospholipid distribution in the lipid bilayer by flippases and scramblases [5]
- Research article Cardiolipin, Mitochondria, and Neurological Disease [6]
- Research article Phosphatidylethanol in blood as a marker of chronic alcohol use: a systematic review and meta-analysis [7]
- Research article Targeting Sphingosine-1-Phosphate Signaling in Immune-Mediated Diseases: Beyond Multiple Sclerosis [8]
- Research article Updating Phospholipase A2 Biology [9]
References
- Chai Z, Zhou Y, Hossain S, Huynh K, Hajimirzaei S, Zhang Y, et al.. Cardiolipin's multifaceted role in immune response: a focus on interacting proteins. . 2025. PMID 41438747 · DOI · PMC12719303
- Poliezhaieva T, Li Y, Chaudhari PS, Isildak U, Alonso-Pernas P, Valentim IS, et al.. Aging-associated decline of phosphatidylcholine synthesis is a malleable trigger of natural mitochondrial aging. . 2026. PMID 42000749 · DOI · PMC13091796
- Cui S, Ye J. Ferroptosis: The Demise of Cells Through Phospholipid Peroxidation. . 2026. PMID 41858270 · DOI · PMC13104129
- Posor Y, Jang W, Haucke V. Phosphoinositides as membrane organizers. Nat Rev Mol Cell Biol. 2022. PMID 35589852 · DOI · PMC9117997
- Sakuragi T, Nagata S. Regulation of phospholipid distribution in the lipid bilayer by flippases and scramblases. Nat Rev Mol Cell Biol. 2023. PMID 37106071 · DOI · PMC10134735
- Falabella M, Vernon HJ, Hanna MG, Claypool SM, Pitceathly RDS. Cardiolipin, Mitochondria, and Neurological Disease. Trends Endocrinol Metab. 2021. PMID 33640250 · DOI · PMC8277580
- Viel G, Boscolo-Berto R, Cecchetto G, Fais P, Nalesso A, Ferrara SD. Phosphatidylethanol in blood as a marker of chronic alcohol use: a systematic review and meta-analysis. Int J Mol Sci. 2012. PMID 23203094 · DOI · PMC3509610
- Pérez-Jeldres T, Alvarez-Lobos M, Rivera-Nieves J. Targeting Sphingosine-1-Phosphate Signaling in Immune-Mediated Diseases: Beyond Multiple Sclerosis. Drugs. 2021. PMID 33983615 · DOI · PMC8116828
- Murakami M, Sato H, Taketomi Y. Updating Phospholipase A2 Biology. Biomolecules. 2020. PMID 33086624 · DOI · PMC7603386
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.