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 (570 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 generic term for fats and lipoids, the alcohol-ether-soluble constituents of protoplasm, which are insoluble in water. They comprise the fats, fatty oils, essential oils, waxes, phospholipids, glycolipids, sulfolipids, aminolipids, chromolipids (lipochromes), and fatty acids. (Grant and Hackh's Chemical Dictionary, 5th ed)
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: Lipid.
Where it fits in the MeSH classification
- Broader topics
- Chemicals and Drugs Category
- Narrower topics
- Ceroid; Fats; Fatty Acids; Fatty Alcohols; Glycerides; Glycolipids; Lipid Peroxides; Lipofuscin; Lipopeptides; Lipopolysaccharides; Lipoproteins; Membrane Lipids; Oils; Polyhydroxyalkanoates
- See also
- Hypolipidemic Agents; Fats; Hyperlipidemias
Research landscape
PubMed indexes 1,393,216 records tagged with the MeSH heading “Lipids” (counts retrieved 2026-10-31). 232,500 of them (16.7%) were published from 2020 onward, and the busiest period so far is through 1999 with 531,480 records.
Reviews account for 115,326 records (8.3%) and meta-analyses for 7,054. Randomized controlled trials number 46,295 (3.3%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 531,480 |
| 2000-2009 | 278,588 |
| 2010-2019 | 350,648 |
| 2020 onward | 232,500 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 115,326 | 8.3% |
| Meta-analyses | 7,054 | 0.5% |
| Randomized controlled trials | 46,295 | 3.3% |
Method: PubMed query "Lipids"[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 deficiency disrupts electron transport chain and drives steatohepatitis | 2026 | Research article Design not recorded in structured metadata | 5 | cc by PMID 42684124 · DOI · PMC13537762 |
| Membrane Curvature Generation by the Caveolin 8S Complex and the Role of Cholesterol | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42708673 · DOI · PMC13564364 |
| The molecular footprint of valproic acid in human hippocampal organoid | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 42897295 · DOI · PMC13680533 |
Cardiolipin deficiency disrupts electron transport chain and drives steatohepatitis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Metabolic dysfunction-associated steatotic liver disease (MASLD) is a progressive disorder marked by lipid accumulation, leading to metabolic dysfunction-associated steatohepatitis (MASH).
- Closing excerpt
- Thus, low mitochondrial CL disrupts the ETC to promote oxidative stress and contributes to the pathogenesis of MASH.
- 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 (158 words)
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a progressive disorder marked by lipid accumulation, leading to metabolic dysfunction-associated steatohepatitis (MASH). A key feature of the transition to MASH involves oxidative stress resulting from defects in mitochondrial oxidative phosphorylation (OXPHOS). Here, we show that pathological alterations in the lipid composition of the inner mitochondrial membrane (IMM) directly instigate electron transfer inefficiency to promote oxidative stress. Specifically, mitochondrial cardiolipin (CL) was downregulated with MASLD/MASH in humans and in mice. Hepatocyte-specific CL synthase knockout (CLS-LKO) led to spontaneous and robust MASH with extensive steatotic and fibrotic phenotype. Loss of CL paradoxically increased mitochondrial respiratory capacity but also promoted electron leak primarily at sites IIIQO and IIF of the electron transport chain (ETC), reduced the formation of I + III2 + IV respiratory supercomplex, and disrupted the propensity of coenzyme Q to become reduced. Thus, low mitochondrial CL disrupts the ETC to promote oxidative stress and contributes to the pathogenesis of MASH.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42684124 · DOI · PMC13537762
Membrane Curvature Generation by the Caveolin 8S Complex and the Role of Cholesterol [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The protein caveolin-1 (Cav1) is essential in the generation of caveolae, but the mechanism of its action remains unclear.
- Closing excerpt
- These observations lead to the hypothesis that cholesterol is enriched in caveolae not because of specific binding to caveolin, but because it can alleviate curvature stress due to its negative spontaneous curvature and its ability to rapidly flip-flop.
- 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 (267 words)
The protein caveolin-1 (Cav1) is essential in the generation of caveolae, but the mechanism of its action remains unclear. A recent cryo-EM structure revealed an 11-mer of Cav1 (the 8S complex) forming a disk with a flat membrane-facing surface, raising the question of how a flat complex is able to generate positive membrane curvature. Previous implicit-solvent and all-atom molecular dynamics simulations showed the 8S complex adopting a conical shape. Here, we simulated the complex in discontinuous membrane patches on the Anton 3 supercomputer. In a 2-μs simulation, a flat POPC membrane patch converted into a hemisphere with the 8S complex on its apex. When the complex was constrained to remain flat, the membrane patch acquired slightly negative curvature. Thus, the conical shape of the 8S complex is essential for positive curvature generation, supporting a scaffolding mechanism of membrane curvature generation by Cav1. The two recently discovered invertebrate caveolins remained flat and generated pronounced negative curvature due to interactions of lipids with the protein rim. Simulations of Cav1 in 70:30 POPC:cholesterol and other cholesterol-containing mixtures showed significantly lower curvature than in the pure POPC membrane or in an E. coli membrane mimic. This appears to be caused by cholesterol moving from the distal to the proximal leaflet. No specific binding of cholesterol to the Cav1 CRAC motif was observed, nor was significant enrichment of cholesterol in contact with the complex. These observations lead to the hypothesis that cholesterol is enriched in caveolae not because of specific binding to caveolin, but because it can alleviate curvature stress due to its negative spontaneous curvature and its ability to rapidly flip-flop.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42708673 · DOI · PMC13564364
The molecular footprint of valproic acid in human hippocampal organoid [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Autism spectrum disorder (ASD) is a multifaceted neurodevelopmental condition characterized by neuroinflammation, and disruption in neuronal development.
- Closing excerpt
- These findings highlight the contribution of miRNA-mediated regulatory mRNA networks to VPA-induced neuroinflammation-associated with ASD in hHOs.
- 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)
Autism spectrum disorder (ASD) is a multifaceted neurodevelopmental condition characterized by neuroinflammation, and disruption in neuronal development. Valproic acid (VPA) is a known environmental risk factor for ASD. Induced pluripotent stem cells (IPSCs IMR90-4)-derived human hippocampal organoids (hHOs) at 60 days of development were used to investigate VPA-induced changes in mRNA and microRNA (miRNA) profiles. The molecular effects of VPA on hHOs were deciphered by meaningfully integrating the ability of miRNA to regulate expression of their predicted mRNA targets crucial to altering neuroinflammatory pathways. Molecular footprint can be defined as the VPA-induced changes to the miRNA profile resulting in coordinated post-transcriptional (mRNA) regulation of neuronal and inflammatory pathways associated with ASD. Based on the results, the molecular footprint of VPA in hHOs was generated for the first time. These findings highlight the contribution of miRNA-mediated regulatory mRNA networks to VPA-induced neuroinflammation-associated with ASD in hHOs.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42897295 · DOI · PMC13680533
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 Atherogenic index of plasma and coronary artery disease: a systematic review and meta-analysis of observational studies [4]
- Research article Triglyceride-glucose-body mass index and the incidence of cardiovascular diseases: a meta-analysis of cohort studies [5]
- Research article Association of triglyceride glucose-body mass index (TyG-BMI) with metabolic dysfunction-associated steatotic liver disease: A systematic review and meta-analysis [6]
- Research article Association between omega-3 fatty acid intake and risk of diabetic retinopathy: A systematic review and meta-analysis [7]
- Research article Vitamin D supplementation vs. placebo and incident type 2 diabetes in an ancillary study of the randomized Vitamin D and Omega-3 Trial [8]
- Research article Effect of lipid-lowering therapies on lipoprotein(a) levels: a comprehensive meta-analysis of randomized controlled trials [9]
References
- Brothwell MJ, Cao G, Maschek JA, Poss AM, Peterlin AD, Wang L, et al.. Cardiolipin deficiency disrupts electron transport chain and drives steatohepatitis. . 2026. PMID 42684124 · DOI · PMC13537762
- Vasquez Rodriguez SY, Lazaridis T. Membrane Curvature Generation by the Caveolin 8S Complex and the Role of Cholesterol. . 2026. PMID 42708673 · DOI · PMC13564364
- Pokharel BR, Cook PP, Akula SM. The molecular footprint of valproic acid in human hippocampal organoid. . 2026. PMID 42897295 · DOI · PMC13680533
- Assempoor R, Daneshvar MS, Taghvaei A, Abroy AS, Azimi A, Nelson JR, et al.. Atherogenic index of plasma and coronary artery disease: a systematic review and meta-analysis of observational studies. Cardiovasc Diabetol. 2025. PMID 39844262 · DOI · PMC11756160
- Rao X, Xin Z, Yu Q, Feng L, Shi Y, Tang T, et al.. Triglyceride-glucose-body mass index and the incidence of cardiovascular diseases: a meta-analysis of cohort studies. Cardiovasc Diabetol. 2025. PMID 39844258 · DOI · PMC11756031
- Boushehri YG, Meymanatabadi Z, Tanha AE, Azami P, Alaei M, Alamdari AA, et al.. Association of triglyceride glucose-body mass index (TyG-BMI) with metabolic dysfunction-associated steatotic liver disease: A systematic review and meta-analysis. PLoS One. 2025. PMID 40758732 · DOI · PMC12321072
- Chen KY, Chan HC, Chan CM. Association between omega-3 fatty acid intake and risk of diabetic retinopathy: A systematic review and meta-analysis. J Nutr Health Aging. 2025. PMID 40987202 · DOI · PMC12492007
- Tobias DK, Pradhan AD, Duran EK, Li C, Song Y, Buring JE, et al.. Vitamin D supplementation vs. placebo and incident type 2 diabetes in an ancillary study of the randomized Vitamin D and Omega-3 Trial. Nat Commun. 2025. PMID 40199888 · DOI · PMC11978796
- Xie S, Galimberti F, Olmastroni E, Carugo S, Catapano AL, Casula M, et al.. Effect of lipid-lowering therapies on lipoprotein(a) levels: a comprehensive meta-analysis of randomized controlled trials. Atherosclerosis. 2025. PMID 40618457 · 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.