GO:0071401 cellular response to triglyceride: Lipid Droplet Signaling, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0071401 (cellular response to triglyceride) describes how a cell changes its state or activity in response to a triglyceride (triacylglycerol) stimulus, including changes in gene expression, secretion, movement and enzyme production.
• Triglycerides are stored in lipid droplets, and their hydrolysis (lipolysis) releases fatty acids that feed mitochondrial metabolism and can also act as signaling molecules.
• Triglyceride breakdown from lipid droplets regulates inflammatory responses in macrophages, linking lipid flux to innate immunity.
• APOE and APOE4 influence triglyceride saturation, lipid droplet size and microglial inflammatory phenotypes, connecting triglyceride handling to Alzheimer disease biology.
• Triacylglycerol mobilization is required for recovery from mitochondrial stress, showing that triglyceride turnover is part of a cellular stress-recovery program.
• The integrated stress response regulates central carbon metabolism and lipid droplet biogenesis, placing triglyceride responses downstream of stress-sensing pathways.
Description
GO:0071401, cellular response to triglyceride, is a biological process Gene Ontology term defined as any process that results in a change in state or activity of a cell (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a triglyceride stimulus. Triglycerides, also called triacylglycerols or triacylglycerides, are neutral lipids stored in cytoplasmic lipid droplets and are central to energy homeostasis. When cells encounter triglyceride-rich particles or liberate triglycerides from internal stores, they activate transcriptional, metabolic and inflammatory programs that allow adaptation to lipid availability. For researchers, GO:0071401 is important because it provides a controlled vocabulary to annotate and interpret experiments in lipid metabolism, immunometabolism and neurodegeneration. Triglyceride breakdown from lipid droplets regulates the inflammatory response in macrophages, demonstrating that this GO term captures physiologically meaningful signaling events rather than only housekeeping lipid storage. Similarly, APOE traffics to astrocyte lipid droplets and modulates triglyceride saturation and droplet size, linking a major Alzheimer disease risk gene to triglyceride handling. Because triglyceride responses intersect with autophagy, mitochondrial stress recovery and the integrated stress response, the term is a useful entry point for functional genomics and CRISPR screening. This article summarizes the definition, mechanism, key genes, disease relevance and experimental methods for studying cellular response to triglyceride, with all factual claims supported by the verified literature listed below.
cellular response to triglyceride At A Glance
| GO ID | GO:0071401 |
|---|---|
| GO term | cellular response to triglyceride |
| Ontology | biological_process |
| Synonyms | cellular response to triacylglyceride; cellular response to triacylglycerol |
| Definition | Any process that results in a change in state or activity of a cell (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a triglyceride stimulus. |
| Major function | Coupling triglyceride availability or mobilization to cellular adaptation, including metabolic, inflammatory and stress-recovery programs. |
| Key organelles | Lipid droplets, mitochondria, lysosomes/autophagosomes and the secretory system. |
| Representative stimuli | Triglyceride-rich lipoproteins, intracellular lipid droplet-derived triglycerides and fatty acid flux. |
| Disease relevance | Inflammation, atherosclerosis, Alzheimer disease and mitochondrial stress-related pathology. |
What Is GO:0071401?
Cellular response to triglyceride (GO:0071401) is the collection of cellular processes triggered when a cell receives a triglyceride stimulus. According to the QuickGO definition, it is any process that results in a change in state or activity of a cell, such as movement, secretion, enzyme production or gene expression, as a result of a triglyceride stimulus. The term has synonyms cellular response to triacylglyceride and cellular response to triacylglycerol. It is a biological_process term and should be distinguished from triglyceride metabolic process, which describes the chemical conversion of triglycerides; GO:0071401 instead describes the cellular reaction to the presence or mobilization of triglycerides.
Why Is cellular response to triglyceride Important in Cell Biology?
Cellular response to triglyceride matters because triglycerides are not merely inert energy stores; their mobilization and sensing influence inflammation, mitochondrial function and cell survival. Triglyceride breakdown from lipid droplets regulates the inflammatory response in macrophages, showing that this process directly shapes innate immune output. Triacylglycerol mobilization underpins mitochondrial stress recovery, indicating that cells require triglyceride turnover to restore homeostasis after stress. APOE and APOE4 modulate triglyceride saturation and lipid droplet size in astrocytes and microglia, connecting this GO term to Alzheimer disease mechanisms. In addition, triglyceride-rich lipoproteins prime aortic endothelium for an enhanced inflammatory response to TNF-alpha, linking triglyceride responses to vascular disease. Because autophagy regulates lipid metabolism, the term also intersects with lysosomal degradation pathways. Together these findings make GO:0071401 a high-value annotation target for metabolic, immunological and neurodegenerative research.
• Defines how cells sense and respond to triglyceride stimuli, enabling consistent annotation of lipid-response experiments.
• Links lipid droplet hydrolysis to inflammatory signaling in macrophages and other immune cells.
• Connects APOE and APOE4 to triglyceride saturation, lipid droplet size and microglial phenotypes relevant to Alzheimer disease.
• Places triglyceride mobilization in the mitochondrial stress recovery program, relevant to mitochondrial disease and aging.
• Ties the integrated stress response to central carbon metabolism and lipid droplet biogenesis.
• Provides a framework for studying adipocyte biology and fat cell function.
• Explains how triglyceride-rich lipoproteins prime endothelium for enhanced inflammatory responses.
• Supports CRISPR and functional genomics screens for genes controlling lipid handling and immunometabolism.
• Helps interpret multi-omics data in metabolic and neurodegenerative disease models.
• Guides development of experimental models for atherosclerosis, inflammation and neurodegeneration.
What Happens During cellular response to triglyceride?
Triglyceride sensing and lipid droplet recognition
In simple terms: The cell first notices that triglycerides are present or being mobilized.
Cellular response to triglyceride begins when a cell detects a triglyceride stimulus, which may be extracellular, such as triglyceride-rich lipoproteins, or intracellular, such as triglycerides stored in lipid droplets. Lipid droplets are the primary storage organelles for triglycerides, and their surface is decorated with proteins that regulate access of lipases and signaling factors. In macrophages, triglyceride breakdown from lipid droplets is a regulated event that influences the inflammatory response, indicating that sensing of lipid droplet triglycerides is coupled to immune signaling. In astrocytes, APOE traffics to lipid droplets and modulates triglyceride saturation and droplet size, showing that lipid droplet composition is part of the cellular response.
Lipolysis and fatty acid release
In simple terms: Enzymes cut triglycerides into fatty acids that the cell can use or signal with.
A central step in the response is the hydrolysis of triglycerides to release fatty acids and glycerol. Autophagy regulates lipid metabolism and contributes to the delivery of lipids to degradation pathways. Triglyceride breakdown from lipid droplets in macrophages is required for the inflammatory response, demonstrating that lipolytic release of fatty acids is functionally important. Triacylglycerol mobilization underpins mitochondrial stress recovery, indicating that fatty acids released from triglycerides are used to support mitochondrial function during recovery. The integrated stress response can also regulate central carbon metabolism and lipid droplet biogenesis, linking lipolysis to broader metabolic reprogramming.
Metabolic and transcriptional reprogramming
In simple terms: The cell changes which genes and metabolic pathways are active.
Following triglyceride sensing and lipolysis, cells alter gene expression and enzyme production, which is explicitly part of the GO:0071401 definition. Triglyceride metabolism controls inflammation and microglial phenotypes associated with APOE4, indicating that transcriptional and phenotypic changes accompany triglyceride handling. The integrated stress response regulates central carbon metabolism and lipid droplet biogenesis, providing a mechanism by which triglyceride responses are integrated with amino acid and carbon metabolism. In adipocytes, fat cell biology illustrates how triglyceride storage and mobilization are coordinated with endocrine and metabolic outputs.
Inflammatory and stress signaling outputs
In simple terms: Triglyceride signals can turn inflammation up or down and help cells recover from stress.
Cellular response to triglyceride can produce inflammatory outputs. Triglyceride breakdown from lipid droplets regulates the inflammatory response in macrophages, showing a direct link between triglyceride mobilization and cytokine programs. Triglyceride-rich lipoproteins prime aortic endothelium for an enhanced inflammatory response to tumor necrosis factor-alpha, linking extracellular triglyceride stimuli to vascular inflammation. Conversely, triacylglycerol mobilization supports recovery from mitochondrial stress, indicating that triglyceride responses can be protective and restorative. APOE4-associated triglyceride metabolism controls inflammation and microglial phenotypes, connecting this process to neuroinflammation.
Resolution and feedback control
In simple terms: The cell returns to balance by rebuilding or storing triglycerides again.
After triglyceride mobilization, cells can re-esterify fatty acids and rebuild lipid droplets, restoring homeostasis. Autophagy regulates lipid metabolism and contributes to the balance between lipid storage and degradation. The integrated stress response can promote lipid droplet biogenesis, which may serve as a feedback mechanism to buffer fatty acids and limit lipotoxicity. APOE modulates triglyceride saturation and droplet size, suggesting that lipid droplet remodeling is part of the resolution phase. In microglia, triglyceride metabolism controls inflammatory phenotypes, implying that feedback regulation of triglyceride handling influences long-term cell states.
Key Genes Involved in GO:0071401 cellular response to triglyceride
The following genes and proteins have been experimentally linked to cellular response to triglyceride, lipid droplet biology and related inflammatory or stress pathways in the verified literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| APOE | Traffics to astrocyte lipid droplets and modulates triglyceride saturation and droplet size | Alzheimer disease risk gene; astrocyte and microglial lipid droplet models |
| APOE4 | Variant associated with altered triglyceride metabolism, inflammation and microglial phenotypes | Neuroinflammation and Alzheimer disease models |
| ATG genes (autophagy machinery) | Autophagy regulates lipid metabolism and lipid droplet turnover | Knockout and flux studies of lipid degradation |
| Lipases (lipid droplet-associated) | Hydrolyze triglycerides to release fatty acids | Lipolysis and inflammatory response assays |
| Mitochondrial metabolic genes | Support fatty acid oxidation during stress recovery | Mitochondrial stress recovery models |
| Integrated stress response genes | Regulate central carbon metabolism and lipid droplet biogenesis | Stress response and metabolomics studies |
| Adipocyte genes | Control fat cell triglyceride storage and mobilization | Adipocyte differentiation and endocrine studies |
| Endothelial inflammatory genes | Mediate enhanced TNF-alpha response after triglyceride-rich lipoprotein exposure | Vascular inflammation models |
| Macrophage inflammatory genes | Link lipid droplet triglyceride breakdown to cytokine output | Immunometabolism and macrophage models |
| Lipid droplet surface proteins | Regulate droplet size, saturation and access of lipases | Imaging and proteomics of lipid droplets |
| Microglial phenotype genes | Associated with APOE4 and triglyceride metabolism | Microglial activation models |
| Fatty acid trafficking genes | Move released fatty acids to mitochondria or other organelles | Metabolic flux and isotope tracing |
| Lipid droplet biogenesis genes | Promote droplet formation during stress | Stress-induced lipid droplet assays |
| Triglyceride-rich lipoprotein receptors | Mediate endothelial responses to triglyceride-rich particles | Endothelial activation studies |
| Autophagy receptors | Target lipid droplets for lysosomal degradation | Autophagic flux and lipid droplet imaging |
| Cytokine genes (e.g., TNF-alpha pathway) | Amplify inflammatory responses primed by triglycerides | Cytokine secretion assays |
| Mitochondrial stress response genes | Coordinate recovery with triglyceride mobilization | Mitochondrial stress and rescue experiments |
How Is cellular response to triglyceride Regulated?
Cellular response to triglyceride is regulated at multiple levels. Autophagy regulates lipid metabolism, controlling the delivery of lipids to lysosomal degradation and thereby influencing triglyceride turnover. The integrated stress response regulates central carbon metabolism and lipid droplet biogenesis, providing a stress-sensing input into triglyceride storage and mobilization. Triacylglycerol mobilization is required for mitochondrial stress recovery, indicating that mitochondrial status feeds back on triglyceride handling. In macrophages, triglyceride breakdown from lipid droplets is coupled to the inflammatory response, suggesting that immune signaling pathways regulate or are regulated by lipolysis. APOE modulates triglyceride saturation and droplet size, adding a genetic layer of regulation relevant to Alzheimer disease. Triglyceride-rich lipoproteins can prime endothelium for enhanced TNF-alpha responses, showing that extracellular lipid signals also shape the regulatory landscape.
cellular response to triglyceride and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| APOE / APOE4 | Alzheimer disease, neuroinflammation, lipid droplet size and triglyceride saturation | Astrocyte and microglial knockout or knock-in of APOE4 |
| Autophagy genes | Lipid metabolism disorders and impaired lipid droplet turnover | CRISPR knockout of autophagy genes with lipid droplet imaging |
| Lipases | Inflammatory and metabolic disease via triglyceride breakdown | Lipase knockout macrophages and mitochondrial stress recovery assays |
| Integrated stress response genes | Metabolic stress and lipid droplet biogenesis | Point mutations in stress-sensing pathways with metabolomics |
| Endothelial inflammatory genes | Atherosclerosis and vascular inflammation | Endothelial cells exposed to triglyceride-rich lipoproteins with cytokine readouts |
Inflammation and atherosclerosis
Cellular response to triglyceride is directly linked to inflammatory disease. Triglyceride breakdown from lipid droplets regulates the inflammatory response in macrophages, a key cell type in atherosclerosis. Triglyceride-rich lipoproteins prime aortic endothelium for an enhanced inflammatory response to tumor necrosis factor-alpha, providing a mechanism for vascular inflammation in cardiometabolic disease. These findings suggest that genes controlling triglyceride mobilization could be therapeutic targets in inflammatory and atherosclerotic conditions.
Alzheimer disease and neurodegeneration
APOE is the strongest genetic risk factor for late-onset Alzheimer disease, and recent work shows that APOE traffics to astrocyte lipid droplets and modulates triglyceride saturation and droplet size. Triglyceride metabolism controls inflammation and microglial phenotypes associated with APOE4, linking triglyceride handling to neuroinflammation. These studies place GO:0071401 at the intersection of lipid biology and neurodegeneration, supporting research into astrocyte and microglial lipid droplets as disease-relevant models.
Mitochondrial stress and metabolic disease
Triacylglycerol mobilization underpins mitochondrial stress recovery, meaning that defects in triglyceride handling could impair recovery from mitochondrial injury. The integrated stress response regulates central carbon metabolism and lipid droplet biogenesis, connecting triglyceride responses to broader metabolic stress pathways. Autophagy regulates lipid metabolism, and impaired autophagic lipid turnover has been implicated in metabolic dysfunction. Together, these mechanisms are relevant to mitochondrial disease, metabolic syndrome and related disorders.
From cellular response to triglyceride-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does a candidate gene control triglyceride breakdown in macrophages? | CRISPR knockout in macrophage cell lines followed by lipid droplet and cytokine assays |
| Does APOE4 alter triglyceride saturation and droplet size? | Knock-in of APOE4 in astrocytes or microglia with lipidomics and imaging |
| Is a gene required for mitochondrial stress recovery via triglyceride mobilization? | Knockout cells subjected to mitochondrial stress with triacylglycerol mobilization readouts |
| Does the integrated stress response regulate lipid droplet biogenesis? | Point-mutation or knockout models of stress-sensing pathways with metabolomics |
| Can a gene be tagged to track lipid droplet localization? | Tagged knock-in of the endogenous locus with fluorescence imaging |
| Does overexpression of a gene enhance or suppress triglyceride responses? | Overexpression cell models with lipid droplet and inflammatory readouts |
How to Study the cellular response to triglyceride Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Lipid droplet imaging | Droplet number, size and localization | APOE and lipid droplet studies |
| Lipidomics / mass spectrometry | Triglyceride species, saturation and abundance | APOE4 and microglial lipid profiling |
| Autophagic flux assays | Lysosomal lipid degradation | Autophagy and lipid metabolism studies |
| Mitochondrial stress tests | Recovery after mitochondrial injury | Triacylglycerol mobilization experiments |
| Metabolomics and isotope tracing | Central carbon metabolism and lipid biogenesis | Integrated stress response studies |
| Cytokine secretion assays | Inflammatory output | Macrophage and endothelial models |
| CRISPR knockout screens | Gene requirement for triglyceride responses | Functional genomics of lipid handling |
| Transcriptomics (RNA-seq) | Gene expression changes after triglyceride stimulus | Pathway annotation for GO:0071401 |
Lipid droplet imaging and quantification
Imaging-based methods are essential for studying cellular response to triglyceride because lipid droplets are the main storage site. APOE trafficking to astrocyte lipid droplets and modulation of triglyceride saturation and droplet size were demonstrated using lipid droplet imaging and lipid analysis. Macrophage studies of triglyceride breakdown from lipid droplets also rely on visualizing droplet dynamics and correlating them with inflammatory outputs. These approaches can be combined with live-cell imaging to track droplet size, number and composition over time.
Lipidomics and triglyceride profiling
Mass spectrometry-based lipidomics measures triglyceride species, saturation and abundance. APOE modulation of triglyceride saturation and droplet size was characterized using lipid profiling. Triglyceride metabolism in APOE4-associated microglial phenotypes has also been studied with lipid-focused analyses. Lipidomics is therefore a core method for assigning functional annotations to GO:0071401 and for testing CRISPR models.
Metabolic flux and mitochondrial stress assays
Triacylglycerol mobilization underpins mitochondrial stress recovery, so flux assays and mitochondrial stress tests are important. The integrated stress response regulates central carbon metabolism and lipid droplet biogenesis, which can be interrogated with metabolomics and isotope tracing. Autophagy regulates lipid metabolism, and autophagic flux assays help determine whether triglyceride turnover depends on lysosomal degradation. These methods connect triglyceride responses to mitochondrial and carbon metabolism.
Inflammatory and cytokine readouts
Because triglyceride responses influence inflammation, cytokine secretion and inflammatory gene expression are key readouts. Triglyceride breakdown from lipid droplets regulates the inflammatory response in macrophages, which can be measured by cytokine assays. Triglyceride-rich lipoproteins prime aortic endothelium for enhanced TNF-alpha responses, providing an endothelial inflammation model. APOE4-associated triglyceride metabolism controls inflammation and microglial phenotypes, supporting cytokine and phenotype profiling in microglia.
How CRISPR Can Be Used to Study GO:0071401 cellular response to triglyceride
Knockout
CRISPR knockout is used to test whether a gene is required for cellular response to triglyceride. For example, knocking out autophagy genes can reveal their role in lipid metabolism and lipid droplet turnover. Knockout of lipases or lipid droplet-associated proteins can determine whether triglyceride breakdown is needed for inflammatory responses in macrophages. Knockout studies also help establish whether triacylglycerol mobilization is required for mitochondrial stress recovery.
Point Mutation
Point mutation models allow precise testing of residues or regulatory sites within genes involved in triglyceride responses. The integrated stress response regulates central carbon metabolism and lipid droplet biogenesis, and point mutations in stress-sensing pathways can dissect which arms control lipid droplet formation. Point mutations can also be used to model disease-associated variants in genes such as APOE that modulate triglyceride saturation and droplet size.
Knock-in
Knock-in models are valuable for expressing disease-relevant variants or tagged proteins at endogenous loci. APOE4 knock-in in astrocytes or microglia can be used to study triglyceride saturation, droplet size and inflammatory phenotypes. Tagged knock-in of lipid droplet proteins enables tracking of their localization and dynamics during triglyceride responses. Knock-in of reporter alleles can also link triglyceride stimuli to transcriptional outputs.
Overexpression
Overexpression models test whether increasing a gene's activity is sufficient to alter cellular response to triglyceride. Overexpressing APOE or APOE4 can change triglyceride saturation and droplet size in astrocytes. Overexpression of inflammatory mediators in endothelial cells can enhance responses to triglyceride-rich lipoproteins and TNF-alpha. Overexpression combined with lipid droplet and cytokine readouts helps establish sufficiency in triglyceride response pathways.
How EDITGENE Supports cellular response to triglyceride Research
Researchers studying cellular response to triglyceride-related genes often need to determine whether a candidate gene is causally involved in lipid droplet dynamics, inflammatory signaling or stress recovery, rather than merely correlated with them. CRISPR-based perturbation provides a direct way to test causality by removing, mutating, tagging or overexpressing the gene of interest in relevant cell models. EDITGENE supports this workflow with knockout, point-mutation, knock-in, overexpression cell models and CRISPR library screening coupled to bioinformatics analysis.
Contact EDITGENE today to design your custom CRISPR model for cellular response to triglyceride research.
Frequently Asked Questions About cellular response to triglyceride
What is GO:0071401 cellular response to triglyceride?
GO:0071401 is a Gene Ontology biological_process term defined as any process that results in a change in state or activity of a cell (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a triglyceride stimulus.
What is the definition of cellular response to triglyceride?
It is the cellular reaction to a triglyceride (triacylglycerol) stimulus, including changes in gene expression, secretion, movement and enzyme production, as defined by QuickGO and supported by lipid metabolism literature.
What genes are involved in cellular response to triglyceride?
Genes involved include APOE and APOE4, autophagy genes, lipid droplet-associated lipases, integrated stress response genes and inflammatory mediators, based on studies of lipid droplets, macrophages, astrocytes and microglia.
How does triglyceride breakdown affect inflammation?
Triglyceride breakdown from lipid droplets regulates the inflammatory response in macrophages, and triglyceride-rich lipoproteins prime endothelium for enhanced TNF-alpha responses.
What is the role of APOE in triglyceride metabolism?
APOE traffics to astrocyte lipid droplets and modulates triglyceride saturation and droplet size, and APOE4-associated triglyceride metabolism controls inflammation and microglial phenotypes.
Why is triacylglycerol mobilization important for mitochondrial stress recovery?
Triacylglycerol mobilization underpins mitochondrial stress recovery, indicating that fatty acids released from triglycerides support mitochondrial function during recovery.
How does autophagy regulate lipid metabolism?
Autophagy regulates lipid metabolism by delivering lipids and lipid droplets to lysosomal degradation, thereby influencing triglyceride turnover.
What methods are used to study cellular response to triglyceride?
Common methods include lipid droplet imaging, lipidomics, autophagic flux assays, mitochondrial stress tests, metabolomics, cytokine assays and CRISPR screens.
Can CRISPR be used to study triglyceride responses?
Yes, CRISPR knockout, point mutation, knock-in and overexpression models can test gene function in lipid droplet dynamics, inflammation and stress recovery.
Which diseases are linked to cellular response to triglyceride?
Inflammation, atherosclerosis, Alzheimer disease and mitochondrial stress-related conditions have been linked to triglyceride handling and lipid droplet biology.
Conclusion
GO:0071401 cellular response to triglyceride captures how cells adapt to triglyceride stimuli through lipid droplet dynamics, lipolysis, metabolic reprogramming and inflammatory signaling. The verified literature shows that this process is central to macrophage inflammation, APOE/APOE4 biology in astrocytes and microglia, mitochondrial stress recovery and endothelial inflammatory priming. Because triglyceride responses intersect with autophagy and the integrated stress response, they are attractive targets for functional genomics and CRISPR-based perturbation. For researchers, the term provides a precise annotation framework for experiments involving lipid droplets, fatty acid flux and immunometabolism. Combining CRISPR knockout, point mutation, knock-in and overexpression models with lipidomics, imaging and cytokine readouts enables causal testing of candidate genes. EDITGENE supports these workflows with cell model generation, library screening and bioinformatics tailored to cellular response to triglyceride research.
References
- 1. Singh R et al.. 2009. Autophagy regulates lipid metabolism.. Nature 458(7242):1131-5 PMID: 19339967
- 2. van Dierendonck XAMH et al.. 2022. Triglyceride breakdown from lipid droplets regulates the inflammatory response in macrophages.. Proc Natl Acad Sci U S A 119(12):e2114739119 PMID: 35302892
- 3. Windham IA et al.. 2024. APOE traffics to astrocyte lipid droplets and modulates triglyceride saturation and droplet size.. J Cell Biol 223(4) PMID: 38334983
- 4. Stephenson RA et al.. 2025. Triglyceride metabolism controls inflammation and microglial phenotypes associated with APOE4.. Cell Rep 44(7):115961 PMID: 40644302
- 5. Baker ZN et al.. 2025. Triacylglycerol mobilization underpins mitochondrial stress recovery.. Nat Cell Biol 27(2):298-308 PMID: 39779944
- 6. Labbé K et al.. 2024. Specific activation of the integrated stress response uncovers regulation of central carbon metabolism and lipid droplet biogenesis.. Nat Commun 15(1):8301 PMID: 39333061
- 7. Ramsay TG. 1996. Fat cells.. Endocrinol Metab Clin North Am 25(4):847-70 PMID: 8977049
- 8. Ting HJ et al.. 2007. Triglyceride-rich lipoproteins prime aortic endothelium for an enhanced inflammatory response to tumor necrosis factor-alpha.. Circ Res 100(3):381-90 PMID: 17234968
