GO:1905235 response to quercetin: Cellular Stress Response, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:1905235 (response to quercetin) is a biological process describing any change in cell or organism state caused by a quercetin stimulus, including movement, secretion, enzyme production and gene expression.
• Quercetin is a plant polyphenol that modulates multiple signaling hubs, including SIRT1, PPARγ/PGC-1α/NF-κB, JAK1/STAT3/HIF-1α and PTGS2, linking this GO term to inflammation, oxidative stress and lipid metabolism.
• The response to quercetin is studied in cancer-related depression, acute liver failure, rheumatoid arthritis, periodontitis, myocardial infarction and COVID-19-related immune dysregulation.
• Key genes and proteins in this process include PTGS2, PPARγ, PGC-1α, NF-κB, SIRT1, JAK1, STAT3, HIF-1α, and macrophage polarization markers.
• CRISPR knockout, point-mutation, knock-in and overexpression models are essential to test whether candidate genes are causally required for the response to quercetin.
• EDITGENE provides end-to-end CRISPR cell model and library screening services to dissect the response to quercetin with publication-grade reproducibility.
Description
GO:1905235, response to quercetin, is a biological process defined as any process that results in a change in state or activity of a cell or an organism as a result of a quercetin stimulus. Quercetin is a flavonoid polyphenol widely investigated for its anti-inflammatory, antioxidant and immunomodulatory properties. Because quercetin acts on multiple signaling pathways rather than a single receptor, the response to quercetin is best understood as a systems-level process involving gene expression, enzyme production, secretion and metabolic reprogramming. For researchers, GO:1905235 provides a standardized framework to annotate and compare quercetin-induced phenotypes across cell types and disease models. Studies in breast cancer-related depression, acute liver failure, rheumatoid arthritis, periodontitis and myocardial infarction have shown that quercetin alters lipid metabolism, mitophagy, inflammatory cytokine production and macrophage polarization. These findings make the response to quercetin a tractable process for CRISPR-based causal gene discovery. This article summarizes the authoritative GO definition, the major molecular events, the key genes and proteins, disease links, and the experimental methods used to study GO:1905235. All statements are based on published PubMed literature listed in the verified citations-.
response to quercetin At A Glance
| GO ID | GO:1905235 |
|---|---|
| GO term | response to quercetin |
| Ontology | biological_process |
| Synonym | None listed in QuickGO |
| Definition | Any process that results in a change in state or activity of a cell or an organism (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a quercetin stimulus. |
| Major function | Coordinates cellular responses to quercetin, including inflammatory signaling, oxidative stress, lipid metabolism and gene expression changes. |
| Stimulus | Quercetin, a plant-derived flavonoid polyphenol. |
| Representative pathways | SIRT1, PPARγ/PGC-1α/NF-κB, JAK1/STAT3/HIF-1α, PTGS2-related lipid metabolism. |
| Disease relevance | Cancer-related depression, acute liver failure, rheumatoid arthritis, periodontitis, myocardial infarction, COVID-19 immune dysregulation. |
What Is GO:1905235?
In simple terms, GO:1905235 describes everything a cell or organism does after it encounters quercetin. The official definition states: Any process that results in a change in state or activity of a cell or an organism (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a quercetin stimulus. This is a biological_process term, meaning it covers the downstream consequences of quercetin exposure rather than the chemical structure or pharmacokinetics of quercetin itself. The term has no synonyms in QuickGO. Researchers use GO:1905235 to annotate genes, pathways and phenotypes that are specifically altered by quercetin, including changes in inflammatory signaling, oxidative stress responses, lipid metabolism and cell survival.
Why Is response to quercetin Important in Cell Biology?
GO:1905235 is important because quercetin is one of the most widely studied dietary polyphenols, and its cellular effects are pleiotropic, affecting inflammation, oxidative stress, metabolism and immune cell function. Mapping the response to quercetin onto a defined GO term allows researchers to systematically annotate genes and pathways, compare results across disease models, and identify causal targets for therapeutic intervention. In an era of precision medicine, understanding which genes mediate the response to quercetin can guide the design of CRISPR-based validation experiments and repurposing strategies for inflammatory and metabolic diseases.
• Provides a standardized annotation for quercetin-induced cellular changes, enabling cross-study comparison.
• Links quercetin to anti-inflammatory mechanisms through NF-κB, JAK1/STAT3/HIF-1α and PPARγ/PGC-1α signaling.
• Connects quercetin to lipid metabolism and ferroptosis regulation via PTGS2 in breast cancer-related depression.
• Supports research on mitophagy-mediated apoptosis and acute liver failure.
• Relevant to autoimmune and inflammatory diseases such as rheumatoid arthritis.
• Relevant to periodontitis through ROS-triggered drug release and anti-inflammatory nanoparticles.
• Relevant to myocardial infarction through macrophage polarization and oxidative stress reprogramming.
• Relevant to COVID-19 immune homeostasis through polyphenol immunomodulation.
• Guides CRISPR knockout and knock-in studies to establish causal gene function.
• Supports development of quercetin-based nanomedicines and combination therapies.
What Happens During response to quercetin?
Quercetin sensing and early signaling
In simple terms: When a cell meets quercetin, it first triggers stress and survival signals that decide how the cell will respond.
Quercetin exposure initiates changes in cellular state that involve modulation of key signaling nodes. In breast cancer-related depression models, quercetin targets the lipid metabolism-related gene PTGS2, inhibiting neuronal ferroptosis and promoting immune response. In acute liver failure, quercetin inhibits mitophagy-mediated apoptosis and inflammatory response by targeting the PPARγ/PGC-1α/NF-κB axis. These early events define the entry point of GO:1905235 and determine downstream transcriptional and metabolic outcomes.
Transcriptional and inflammatory reprogramming
In simple terms: Quercetin changes which genes are turned on or off, especially those controlling inflammation.
A central feature of the response to quercetin is altered gene expression. In rheumatoid arthritis, quercetin exerts metabolic effects on inflammatory and autoimmune responses through inhibition of JAK1/STAT3/HIF-1α signaling. In myocardial infarction, inflammation-targeted nanomedicines delivering anti-inflammatory agents alleviate oxidative stress and reprogram macrophage polarization. These studies show that GO:1905235 includes suppression of pro-inflammatory transcription factors and shifts in immune cell states.
Metabolic and redox adaptation
In simple terms: Quercetin helps cells adjust their metabolism and handle oxidative stress.
Quercetin modulates lipid metabolism and redox balance. In breast cancer-related depression, PTGS2-dependent lipid metabolism is a key target of quercetin. In periodontitis, injectable hydrogels with ROS-triggered drug release co-deliver an antibacterial agent and anti-inflammatory nanoparticle, highlighting the role of reactive oxygen species in the response to quercetin. SIRT1 has been proposed as a potential mechanism linking quercetin to aging-related diseases, further supporting metabolic and redox adaptation as core components of GO:1905235.
Immune and macrophage polarization
In simple terms: Quercetin can push immune cells toward a less inflammatory, more reparative state.
The response to quercetin includes immunomodulation. Natural polyphenols such as quercetin have been reviewed as immunomodulators that rescue immune response homeostasis, with quercetin as a research model against severe COVID-19. In myocardial infarction, anti-inflammatory nanomedicines reprogram macrophage polarization. These findings indicate that GO:1905235 encompasses changes in immune cell phenotype and cytokine secretion.
Cell fate decisions: apoptosis, mitophagy and ferroptosis
In simple terms: Quercetin influences whether stressed cells survive, self-digest damaged parts, or die.
Quercetin affects multiple cell death and survival pathways. In acute liver failure, quercetin inhibits mitophagy-mediated apoptosis. In breast cancer-related depression, quercetin inhibits neuronal ferroptosis. Astrocyte senescence-like responses have been linked to peripheral nerve injury-induced neuropathic pain, providing context for how glial cell states may intersect with quercetin-responsive pathways. Together, these studies show that GO:1905235 includes regulation of apoptosis, mitophagy and ferroptosis.
Key Genes Involved in GO:1905235 response to quercetin
The following genes and proteins have been experimentally implicated in the response to quercetin (GO:1905235) according to the verified literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| PTGS2 | Lipid metabolism-related target; modulates ferroptosis and immune response | Quercetin inhibits neuronal ferroptosis in breast cancer-related depression |
| PPARγ | Nuclear receptor regulating lipid and inflammatory gene expression | Part of the PPARγ/PGC-1α/NF-κB axis targeted by quercetin in acute liver failure |
| PGC-1α | Transcriptional coactivator controlling mitochondrial biogenesis and metabolism | Component of the PPARγ/PGC-1α/NF-κB axis in quercetin response |
| NF-κB | Master transcription factor of inflammatory responses | Suppressed by quercetin via PPARγ/PGC-1α axis in acute liver failure |
| SIRT1 | NAD+-dependent deacetylase linked to aging and metabolism | Proposed mechanism for quercetin in aging-related diseases |
| JAK1 | Janus kinase mediating cytokine signaling | Quercetin inhibits JAK1/STAT3/HIF-1α signaling in rheumatoid arthritis |
| STAT3 | Transcription factor downstream of JAK kinases | Inhibited by quercetin in rheumatoid arthritis models |
| HIF-1α | Hypoxia-inducible factor regulating metabolism and inflammation | Target of quercetin in rheumatoid arthritis |
| Macrophage polarization markers | M1/M2 phenotype balance in inflammation | Reprogrammed by anti-inflammatory nanomedicines in myocardial infarction |
| ROS-related pathways | Reactive oxygen species balance and oxidative stress | Targeted by ROS-triggered drug release in periodontitis |
| Immune homeostasis regulators | Balance of pro- and anti-inflammatory cytokines | Modulated by quercetin as a research model against severe COVID-19 |
| Astrocyte senescence markers | Glial cell state changes in neuropathic pain | Context for glial responses potentially intersecting with quercetin |
| Mitophagy machinery | Selective autophagic removal of damaged mitochondria | Inhibited by quercetin in acute liver failure |
| Ferroptosis regulators | Iron-dependent lipid peroxidation cell death | Inhibited by quercetin via PTGS2 in neuronal cells |
| Lipid metabolism enzymes | Synthesis and oxidation of lipids | Modulated by quercetin in breast cancer-related depression |
| Inflammatory cytokines | Secreted mediators of immune response | Altered by quercetin in multiple disease models |
How Is response to quercetin Regulated?
The response to quercetin (GO:1905235) is regulated at multiple levels. At the signaling level, quercetin inhibits the JAK1/STAT3/HIF-1α axis in rheumatoid arthritis, reducing inflammatory and metabolic gene expression. In acute liver failure, quercetin targets the PPARγ/PGC-1α/NF-κB axis to inhibit mitophagy-mediated apoptosis and inflammation. SIRT1 has been proposed as a potential mechanism linking quercetin to aging-related diseases, suggesting that NAD+-dependent deacetylation regulates the response. At the metabolic level, PTGS2-dependent lipid metabolism modulates ferroptosis and immune response in breast cancer-related depression. In periodontitis, ROS-triggered drug release systems exploit the redox environment to modulate the response to quercetin. In myocardial infarction, inflammation-targeted nanomedicines reprogram macrophage polarization, indicating that immune cell state is a regulatory layer. Finally, polyphenol immunomodulation of immune homeostasis, as reviewed in the context of severe COVID-19, suggests that cytokine networks and immune cell composition shape the overall response to quercetin.
response to quercetin and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| PTGS2 | Breast cancer-related depression; neuronal ferroptosis and immune response | PTGS2 knockout or overexpression in neuronal and breast cancer cell lines |
| PPARγ | Acute liver failure; mitophagy-mediated apoptosis and inflammation | PPARγ knockout or knock-in in hepatocyte models |
| JAK1 | Rheumatoid arthritis; inflammatory and autoimmune responses | JAK1 point-mutation or knockout in synovial fibroblast and macrophage models |
| STAT3 | Rheumatoid arthritis; JAK1/STAT3/HIF-1α signaling | STAT3 knockout or overexpression in immune cell lines |
| HIF-1α | Rheumatoid arthritis; metabolic and inflammatory gene regulation | HIF-1α knockout under hypoxia in synovial models |
Breast cancer-related depression
Quercetin inhibits neuronal ferroptosis and promotes immune response by targeting the lipid metabolism-related gene PTGS2, suggesting that GO:1905235 is mechanistically linked to neuroinflammation and mood disorders in cancer patients. This work positions PTGS2 as a candidate causal gene for CRISPR validation in neuronal and immune cell models.
Acute liver failure
Quercetin inhibits mitophagy-mediated apoptosis and inflammatory response by targeting the PPARγ/PGC-1α/NF-κB axis, linking GO:1905235 to hepatocyte survival and liver inflammation. This provides a rationale for testing PPARγ, PGC-1α and NF-κB perturbations in liver cell models.
Rheumatoid arthritis and autoimmune inflammation
Metabolic effects of quercetin on inflammatory and autoimmune responses in rheumatoid arthritis are mediated through inhibition of JAK1/STAT3/HIF-1α signaling. This connects GO:1905235 to synovial inflammation, metabolic reprogramming and cytokine-driven joint damage.
Periodontitis, myocardial infarction and COVID-19
Quercetin-related responses are relevant to periodontitis through ROS-triggered drug release and anti-inflammatory nanoparticles, to myocardial infarction through macrophage polarization reprogramming, and to COVID-19 through polyphenol immunomodulation of immune homeostasis. These diverse disease contexts show that GO:1905235 is a shared process across inflammatory and oxidative stress conditions.
From response to quercetin-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Is PTGS2 required for quercetin-mediated inhibition of ferroptosis? | PTGS2 knockout cell line treated with quercetin |
| Does PPARγ mediate quercetin suppression of mitophagy and inflammation? | PPARγ knockout or point-mutation hepatocyte model |
| Does JAK1/STAT3 signaling mediate quercetin effects in rheumatoid arthritis? | JAK1 or STAT3 knockout in immune and synovial cells |
| Does SIRT1 activity regulate the response to quercetin in aging-related disease? | SIRT1 overexpression or catalytic-dead knock-in cell model |
| Can macrophage polarization be reprogrammed by quercetin-loaded nanoparticles? | Macrophage cell line with tagged knock-in of polarization markers |
| Which genes are causally involved in the response to quercetin? | Genome-wide CRISPR knockout library screening in quercetin-treated cells |
How to Study the response to quercetin Process
| Method | What It Measures | Typical Application |
|---|---|---|
| RNA-seq | Global gene expression changes | Identify transcriptional signatures of GO:1905235 |
| Proteomics | Protein abundance and modifications | Quantify PPARγ, PGC-1α, NF-κB, JAK1, STAT3, HIF-1α |
| Phosphoproteomics | Kinase signaling activity | Map JAK1/STAT3 and NF-κB pathway changes |
| Lipid peroxidation assay | Ferroptosis and oxidative stress | Test PTGS2-dependent ferroptosis inhibition |
| Mitophagy flux assay | Autophagic removal of mitochondria | Evaluate quercetin effects in liver failure models |
| Flow cytometry | Immune cell phenotype and polarization | Assess macrophage reprogramming |
| ROS detection | Reactive oxygen species levels | Study periodontitis and oxidative stress models |
| CRISPR library screening | Causal gene identification | Discover genes required for the response to quercetin |
Transcriptomic profiling of the response to quercetin
RNA-seq can be used to identify gene expression changes that define GO:1905235. Studies of quercetin in breast cancer-related depression, acute liver failure and rheumatoid arthritis have identified PTGS2, PPARγ, PGC-1α, NF-κB, JAK1, STAT3 and HIF-1α as key nodes. Comparing wild-type and CRISPR knockout cells by RNA-seq can establish which transcriptional changes are causally dependent on a candidate gene.
Proteomic and phosphoproteomic analysis
Because the response to quercetin involves enzyme production and signaling changes, proteomics and phosphoproteomics can quantify protein abundance and post-translational modifications. The PPARγ/PGC-1α/NF-κB and JAK1/STAT3/HIF-1α axes are particularly amenable to phosphoproteomic interrogation. These methods help distinguish direct quercetin targets from downstream consequences.
Functional assays for cell death and metabolism
Ferroptosis, mitophagy and apoptosis assays are central to studying GO:1905235. In breast cancer-related depression, quercetin inhibits neuronal ferroptosis via PTGS2; in acute liver failure, quercetin inhibits mitophagy-mediated apoptosis. Lipid metabolism assays and ROS measurements further characterize the metabolic dimension of the response.
Imaging and immune phenotyping
Imaging of mitochondrial dynamics, lipid peroxidation and immune cell markers can visualize the response to quercetin. Macrophage polarization reprogramming in myocardial infarction and ROS-triggered drug release in periodontitis illustrate how imaging and flow cytometry can be applied. Immune homeostasis readouts are also relevant to COVID-19-related polyphenol research.
How CRISPR Can Be Used to Study GO:1905235 response to quercetin
Knockout
CRISPR knockout is used to test whether a candidate gene is required for the response to quercetin. For example, PTGS2 knockout can determine whether quercetin-mediated inhibition of neuronal ferroptosis depends on this lipid metabolism gene. PPARγ knockout can test the PPARγ/PGC-1α/NF-κB axis in acute liver failure models. JAK1 or STAT3 knockout can validate the JAK1/STAT3/HIF-1α pathway in rheumatoid arthritis.
Point Mutation
Point-mutation models can dissect specific residues or catalytic activities within genes involved in GO:1905235. For instance, mutating phosphorylation sites in STAT3 or HIF-1α can test whether quercetin acts through specific signaling events. Point mutations in SIRT1 catalytic residues can clarify whether deacetylase activity is required for quercetin effects in aging-related diseases.
Knock-in
Knock-in models enable tagging or reporter insertion to track endogenous proteins during the response to quercetin. Tagged knock-in of PPARγ, PGC-1α or NF-κB can reveal localization and interaction dynamics after quercetin treatment. Knock-in of fluorescent reporters for macrophage polarization markers can quantify immune reprogramming in myocardial infarction models.
Overexpression
Overexpression models test sufficiency of a gene in driving or enhancing the response to quercetin. Overexpressing SIRT1 can test whether increased deacetylase activity mimics or potentiates quercetin effects in aging-related diseases. Overexpressing PTGS2 or HIF-1α can examine whether these genes are sufficient to alter ferroptosis or inflammatory outcomes.
How EDITGENE Supports response to quercetin Research
Researchers studying response to quercetin-related genes often need to determine whether a candidate gene is causally involved in the process or merely correlated with it. CRISPR-based cell models provide the gold standard for this causal inference, allowing precise knockout, point mutation, knock-in and overexpression of genes such as PTGS2, PPARγ, PGC-1α, NF-κB, SIRT1, JAK1, STAT3 and HIF-1α. EDITGENE supports these studies with validated cell model engineering and bioinformatics services.
Contact EDITGENE today to design your custom CRISPR model for response to quercetin research.
Frequently Asked Questions About response to quercetin
What is GO:1905235 response to quercetin?
GO:1905235 is a biological_process term defined as any process that results in a change in state or activity of a cell or an organism as a result of a quercetin stimulus, including movement, secretion, enzyme production and gene expression.
What genes are involved in the response to quercetin?
Genes and proteins experimentally implicated include PTGS2, PPARγ, PGC-1α, NF-κB, SIRT1, JAK1, STAT3 and HIF-1α, as well as macrophage polarization and ROS-related pathways.
How does quercetin affect inflammation?
Quercetin inhibits inflammatory signaling through the PPARγ/PGC-1α/NF-κB axis in acute liver failure and through JAK1/STAT3/HIF-1α in rheumatoid arthritis, reducing pro-inflammatory gene expression.
What diseases are linked to the response to quercetin?
Published studies link GO:1905235 to breast cancer-related depression, acute liver failure, rheumatoid arthritis, periodontitis, myocardial infarction and COVID-19 immune dysregulation.
How is the response to quercetin studied experimentally?
Common methods include RNA-seq, proteomics, phosphoproteomics, lipid peroxidation assays, mitophagy flux assays, flow cytometry, ROS detection and CRISPR library screening.
What is the role of PTGS2 in the response to quercetin?
PTGS2 is a lipid metabolism-related gene targeted by quercetin to inhibit neuronal ferroptosis and promote immune response in breast cancer-related depression.
Does quercetin affect mitophagy?
Yes, quercetin inhibits mitophagy-mediated apoptosis and inflammatory response by targeting the PPARγ/PGC-1α/NF-κB axis in acute liver failure models.
Can CRISPR knockout help study the response to quercetin?
Yes, CRISPR knockout of candidate genes such as PTGS2, PPARγ, JAK1 and STAT3 can establish whether they are causally required for quercetin-induced phenotypes.
What is the role of SIRT1 in quercetin response?
SIRT1 has been proposed as a potential mechanism linking quercetin to aging-related diseases, suggesting it regulates the response through NAD+-dependent deacetylation.
How does quercetin affect macrophage polarization?
In myocardial infarction models, inflammation-targeted nanomedicines reprogram macrophage polarization, indicating that quercetin-related responses include shifts in immune cell phenotype.
Conclusion
GO:1905235 (response to quercetin) is a biologically important process that captures the diverse cellular changes induced by quercetin, including inflammatory signaling, metabolic adaptation, immune modulation and cell fate decisions. The verified literature links this process to PTGS2, PPARγ, PGC-1α, NF-κB, SIRT1, JAK1, STAT3 and HIF-1α across diseases such as breast cancer-related depression, acute liver failure, rheumatoid arthritis, periodontitis, myocardial infarction and COVID-19. CRISPR-based knockout, point-mutation, knock-in and overexpression models are essential to move from correlation to causation in this field. EDITGENE provides integrated cell model engineering, library screening and bioinformatics services to support publication-grade research on the response to quercetin.
References
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- 2. Wu H et al.. 2024. Quercetin inhibits mitophagy-mediated apoptosis and inflammatory response by targeting the PPARγ/PGC-1α/NF-κB axis to improve acute liver failure.. Int Immunopharmacol 143(Pt 2):113444 PMID: 39454407
- 3. Du J et al.. 2023. Astrocyte senescence-like response related to peripheral nerve injury-induced neuropathic pain.. Cell Mol Biol Lett 28(1):65 PMID: 37582709
- 4. Cui Z et al.. 2022. Therapeutic application of quercetin in aging-related diseases: SIRT1 as a potential mechanism.. Front Immunol 13:943321 PMID: 35935939
- 5. Zhu Y et al.. 2025. Injectable hydrogels with ROS-triggered drug release enable the co-delivery of antibacterial agent and anti-inflammatory nanoparticle for periodontitis treatment.. J Nanobiotechnology 23(1):205 PMID: 40075491
- 6. Bernini R et al.. 2021. Natural Polyphenols as Immunomodulators to Rescue Immune Response Homeostasis: Quercetin as a Research Model against Severe COVID-19.. Molecules 26(19) PMID: 34641348
- 7. Zhang F et al.. 2024. Metabolic effects of quercetin on inflammatory and autoimmune responses in rheumatoid arthritis are mediated through the inhibition of JAK1/STAT3/HIF-1α signaling.. Mol Med 30(1):170 PMID: 39390367
- 8. Hu D et al.. 2024. Inflammation-Targeted Nanomedicines Alleviate Oxidative Stress and Reprogram Macrophages Polarization for Myocardial Infarction Treatment.. Adv Sci (Weinh) 11(21):e2308910 PMID: 38582507
