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 (635 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
Derivatives of phosphatidic acid in which the hydrophobic regions are composed of two fatty acids and a polar alcohol is joined to the C-3 position of glycerol through a phosphodiester bond. They are named according to their polar head groups, such as phosphatidylcholine and phosphatidylethanolamine.
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: Glycerophospholipid; Phosphoglyceride; Phosphoglycerides.
Where it fits in the MeSH classification
- Broader topics
- Phosphatidic Acids
- Narrower topics
- Glycerylphosphorylcholine; Phosphatidylcholines; Phosphatidylethanolamines; Phosphatidylglycerols; Phosphatidylinositols; Phosphatidylserines; Phospholipid Ethers
Research landscape
PubMed indexes 94,360 records tagged with the MeSH heading “Glycerophospholipids” (counts retrieved 2026-10-31). 8,939 of them (9.5%) were published from 2020 onward, and the busiest period so far is through 1999 with 48,448 records.
Reviews account for 5,884 records (6.2%) and meta-analyses for 39. Randomized controlled trials number 593 (0.6%) 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 | 48,448 |
| 2000-2009 | 18,615 |
| 2010-2019 | 18,358 |
| 2020 onward | 8,939 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 5,884 | 6.2% |
| Meta-analyses | 39 | 0.0% |
| Randomized controlled trials | 593 | 0.6% |
Method: PubMed query "Glycerophospholipids"[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 |
|---|---|---|---|---|
| Targeting Lp-PLA2 inhibits profibrotic monocyte-derived macrophages in silicosis through restoring cardiolipin-mediated mitophagy | 2025 | Research article Design not recorded in structured metadata | 33 | cc by PMID 40389600 · DOI · PMC12206922 |
| ATG9A and ARFIP2 cooperate to control PI4P levels for lysosomal repair | 2025 | Research article Design not recorded in structured metadata | 30 | cc by PMID 40460835 · DOI · PMC7617826 |
| The Vps13-like protein BLTP2 regulates phosphatidylethanolamine levels to maintain plasma membrane fluidity and breast cancer aggressiveness | 2025 | Research article Design not recorded in structured metadata | 25 | cc by PMID 40579455 · DOI · PMC12270902 |
| 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 |
Targeting Lp-PLA2 inhibits profibrotic monocyte-derived macrophages in silicosis through restoring cardiolipin-mediated mitophagy [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Monocyte-derived macrophages (MoMacs) are the most important effector cells that cause pulmonary fibrosis.
- Closing excerpt
- Our findings enhance our understanding of silicosis pathogenesis and offer promising opportunities for developing targeted therapies to mitigate fibrotic progression and maintain lung function in affected individuals.
- 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 (202 words)
Monocyte-derived macrophages (MoMacs) are the most important effector cells that cause pulmonary fibrosis. However, the characteristics of MoMac differentiation in silicosis and the mechanisms by which MoMacs affect the progression of pulmonary fibrosis remain unclear. Integration of single-cell and spatial transcriptomic analyses revealed that the silicosis niche was occupied by a subset of MoMacs, identified as Spp1hiMacs, which remain in an immature transitional state of differentiation during silicosis. This study investigated the mechanistic foundations of mitochondrial damage induced by the lipoprotein-associated phospholipase A2 (Lp-PLA2, encoded by Pla2g7)-acyl-CoA:lysocardiolipin acyltransferase-1 (ALCAT1)-cardiolipin (CL) signaling pathway, which interferes with Spp1hiMac differentiation. We demonstrated that in SiO2-induced MoMacs, Lp-PLA2 induces abnormal CL acylation through the activation of ALCAT1, resulting in impaired mitochondrial localization of PINK1 and LC3B and mitochondrial autophagy defects. Simultaneously, lysosomal dysfunction causes the release of the lysosomal protein cathepsin B into the cytoplasm, which involves M1 and M2 macrophage polarization and the activation of proinflammatory and profibrotic pathways. Furthermore, we assessed the efficacy of the Lp-PLA2 inhibitor darapladib in ameliorating silica-induced pulmonary fibrosis in a murine model. Our findings enhance our understanding of silicosis pathogenesis and offer promising opportunities for developing targeted therapies to mitigate fibrotic progression and maintain lung function in affected individuals.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40389600 · DOI · PMC12206922
ATG9A and ARFIP2 cooperate to control PI4P levels for lysosomal repair [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Lysosome damage activates multiple pathways to prevent lysosome-dependent cell death, including a repair mechanism involving endoplasmic reticulum (ER)-lysosome membrane contact sites, phosphatidylinositol 4-kinase-2a (PI4K2A), phosphatidylinositol-4 phosphate (PI4P), and oxysterol-binding protein-like proteins (OSBPLs) lipid transfer proteins.
- Closing excerpt
- Our results identify a role for mobilized ATG9A vesicles and ARFIP2 in lysosome homeostasis after damage and bacterial infection.
- 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 (135 words)
Lysosome damage activates multiple pathways to prevent lysosome-dependent cell death, including a repair mechanism involving endoplasmic reticulum (ER)-lysosome membrane contact sites, phosphatidylinositol 4-kinase-2a (PI4K2A), phosphatidylinositol-4 phosphate (PI4P), and oxysterol-binding protein-like proteins (OSBPLs) lipid transfer proteins. PI4K2A localizes to the trans-Golgi network and endosomes, yet how it is delivered to damaged lysosomes remains unknown. During acute sterile damage and damage caused by intracellular bacteria, we show that ATG9A-containing vesicles perform a critical role in delivering PI4K2A to damaged lysosomes. ADP ribosylation factor interacting protein 2 (ARFIP2), a component of ATG9A vesicles, binds and sequesters PI4P on lysosomes, balancing OSBPL-dependent lipid transfer and promoting the retrieval of ATG9A vesicles through the recruitment of the adaptor protein complex-3 (AP-3). Our results identify a role for mobilized ATG9A vesicles and ARFIP2 in lysosome homeostasis after damage and bacterial infection.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40460835 · DOI · PMC7617826
The Vps13-like protein BLTP2 regulates phosphatidylethanolamine levels to maintain plasma membrane fluidity and breast cancer aggressiveness [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Lipid transport proteins (LTPs) facilitate non-vesicular lipid exchange between cellular compartments and have critical roles in lipid homeostasis.
- Closing excerpt
- We found that BLTP2 facilitates growth of a triple negative breast cancer cell line and sustains its aggressiveness in an in vivo model of metastasis, suggesting maintenance of PM fluidity by BLTP2 may be critical for tumorigenesis in humans.
- 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 (152 words)
Lipid transport proteins (LTPs) facilitate non-vesicular lipid exchange between cellular compartments and have critical roles in lipid homeostasis. A recently identified family of bridge-like LTPs (BLTPs) is thought to form lipid-transporting conduits between organelles. One of these, BLTP2, is conserved across species but its function is not known. Here we show that BLTP2 regulates plasma membrane (PM) fluidity by increasing phosphatidylethanolamine (PE) levels in the PM. BLTP2 localizes to endoplasmic reticulum (ER)-PM contact sites, and transports PE in vivo, suggesting it drives PE movement from ER to PM. We find that BLTP2 works in parallel with another pathway that regulates intracellular PE distribution and PM fluidity. BLTP2 expression correlates with breast cancer aggressiveness. We found that BLTP2 facilitates growth of a triple negative breast cancer cell line and sustains its aggressiveness in an in vivo model of metastasis, suggesting maintenance of PM fluidity by BLTP2 may be critical for tumorigenesis in humans.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40579455 · DOI · PMC12270902
Aging-associated decline of phosphatidylcholine synthesis is a malleable trigger of natural mitochondrial aging [4]
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
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 The critical role of phosphatidylcholine and phosphatidylethanolamine metabolism in health and disease [5]
- Research article Exosomal lipid composition and the role of ether lipids and phosphoinositides in exosome biology [6]
- Research article The mechanisms of lysophosphatidylcholine in the development of diseases [7]
- Research article Phosphoinositides as membrane organizers [8]
- Research article Cardiolipin, Mitochondria, and Neurological Disease [9]
- Research article Structural and functional consequences of reversible lipid asymmetry in living membranes [10]
References
- Li S, Xu H, Liu S, Hou J, Han Y, Li C, et al.. Targeting Lp-PLA2 inhibits profibrotic monocyte-derived macrophages in silicosis through restoring cardiolipin-mediated mitophagy. . 2025. PMID 40389600 · DOI · PMC12206922
- De Tito S, Almacellas E, Dai Yu D, Millard E, Zhang W, de Heus C, et al.. ATG9A and ARFIP2 cooperate to control PI4P levels for lysosomal repair. . 2025. PMID 40460835 · DOI · PMC7617826
- Banerjee S, Daetwyler S, Bai X, Michaud M, Jouhet J, Binns D, et al.. The Vps13-like protein BLTP2 regulates phosphatidylethanolamine levels to maintain plasma membrane fluidity and breast cancer aggressiveness. . 2025. PMID 40579455 · DOI · PMC12270902
- 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
- van der Veen JN, Kennelly JP, Wan S, Vance JE, Vance DE, Jacobs RL. The critical role of phosphatidylcholine and phosphatidylethanolamine metabolism in health and disease. Biochim Biophys Acta Biomembr. 2017. PMID 28411170 · DOI
- Skotland T, Hessvik NP, Sandvig K, Llorente A. Exosomal lipid composition and the role of ether lipids and phosphoinositides in exosome biology. J Lipid Res. 2019. PMID 30076207 · DOI · PMC6314266
- Liu P, Zhu W, Chen C, Yan B, Zhu L, Chen X, et al.. The mechanisms of lysophosphatidylcholine in the development of diseases. Life Sci. 2020. PMID 32084434 · DOI
- Posor Y, Jang W, Haucke V. Phosphoinositides as membrane organizers. Nat Rev Mol Cell Biol. 2022. PMID 35589852 · DOI · PMC9117997
- Falabella M, Vernon HJ, Hanna MG, Claypool SM, Pitceathly RDS. Cardiolipin, Mitochondria, and Neurological Disease. Trends Endocrinol Metab. 2021. PMID 33640250 · DOI · PMC8277580
- Doktorova M, Symons JL, Levental I. Structural and functional consequences of reversible lipid asymmetry in living membranes. Nat Chem Biol. 2020. PMID 33199908 · DOI · PMC7747298
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.