GO:1905523 positive regulation of macrophage migration: Signaling Pathways, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:1905523 (positive regulation of macrophage migration) describes any process that activates or increases the frequency, rate, or extent of macrophage migration, a critical step in inflammation, tissue repair, and tumor progression [1, 3, 7].
• Macrophage migration is driven by chemokine gradients, metabolic cues, and extracellular matrix remodeling, with key regulators including osteopontin, GPR65, PIEZO1, and DOCK7 [1, 3, 5, 7].
• Tumor-associated macrophages (TAMs) exploit positive regulation of migration to infiltrate glioblastoma, breast cancer, colorectal cancer, and other malignancies, making this process a therapeutic target [1, 2, 7].
• Metabolic reprogramming, such as glycolysis and cholesterol metabolism, directly promotes macrophage migration and polarization, linking cellular metabolism to migratory capacity [2, 6].
• CRISPR-based models (knockout, point mutation, knock-in, overexpression) enable precise dissection of genes that positively regulate macrophage migration [1, 4, 5].
• Targeting positive regulators of macrophage migration, such as ILT4 or osteopontin, can enhance anti-PD-L1 therapy and reduce pathological neovascularization [4, 8].
Description
Macrophages are innate immune cells that migrate to sites of infection, injury, and tumor growth, where they perform diverse functions ranging from pathogen clearance to tissue remodeling [1, 3]. The process by which macrophages are stimulated to move more frequently, faster, or farther is formally described by the Gene Ontology term GO:1905523, positive regulation of macrophage migration [1, 5]. This biological process is essential for mounting effective immune responses, but its dysregulation contributes to chronic inflammation, cancer progression, and aberrant angiogenesis [3, 7, 8]. Understanding the molecular players that positively regulate macrophage migration is therefore a central goal in immunology and oncology research. Recent studies have identified numerous positive regulators of macrophage migration, including secreted factors like osteopontin, which mediates glioblastoma-associated macrophage infiltration, and IL6, which activates PIEZO1 to promote M1 macrophage migration in orthodontic root resorption. Metabolic signals also play a key role: GPR65 senses tumor-derived lactate to induce HMGB1 release from TAMs and promote glioma progression, while Zeb1-induced glycolytic reprogramming is essential for macrophage polarization in breast cancer. These findings highlight the diversity of mechanisms that converge on positive regulation of macrophage migration. For researchers, GO:1905523 provides a standardized framework to annotate and study genes, pathways, and experimental models that enhance macrophage motility. This article synthesizes authoritative QuickGO data and verified PubMed literature to deliver a publication-ready overview of the term, its mechanisms, associated genes, disease relevance, and CRISPR-based research strategies.
positive regulation of macrophage migration At A Glance
| GO ID | GO:1905523 |
|---|---|
| GO term | positive regulation of macrophage migration |
| Ontology | biological_process |
| Synonym | activation of macrophage migration; up regulation of macrophage migration; up-regulation of macrophage migration; upregulation of macrophage migration |
| Definition | Any process that activates or increases the frequency, rate or extent of macrophage migration. |
| Major function | Enhances the directed movement of macrophages, critical for inflammation, immune surveillance, tissue repair, and tumor progression. |
| Related processes | Chemotaxis, cell migration, macrophage activation, cytokine signaling, metabolic reprogramming. |
| Key regulators | Osteopontin, GPR65, PIEZO1, DOCK7, ILT4, Zeb1, CircABCA1, TREM2. |
| Disease relevance | Cancer (glioblastoma, breast, colorectal, ccRCC), retinal neovascularization, orthodontic root resorption. |
What Is GO:1905523?
According to the Gene Ontology, GO:1905523 (positive regulation of macrophage migration) is defined as any process that activates or increases the frequency, rate, or extent of macrophage migration. It is a biological process that encompasses molecular signals, cellular changes, and environmental cues that enhance the movement of macrophages from one location to another. Synonyms include activation of macrophage migration, up regulation of macrophage migration, up-regulation of macrophage migration, and upregulation of macrophage migration.
Why Is positive regulation of macrophage migration Important in Cell Biology?
Positive regulation of macrophage migration is a fundamental process in both health and disease. It enables macrophages to rapidly reach sites of infection or injury, thereby initiating and resolving inflammation [1, 5]. In cancer, however, enhanced macrophage migration promotes tumor infiltration and progression, as seen in glioblastoma, breast cancer, and colorectal cancer [1, 2, 7]. Understanding the molecular mechanisms that positively regulate this process can reveal therapeutic targets to modulate immune responses, enhance cancer immunotherapy, and treat inflammatory or neovascular diseases [4, 8].
• Essential for innate immune responses: macrophages must migrate to infection sites to eliminate pathogens and initiate tissue repair [1, 5].
• Drives tumor progression: TAM infiltration into glioblastoma, breast cancer, and colorectal cancer depends on positive regulation of macrophage migration [1, 2, 7].
• Metabolic control: glycolysis and cholesterol metabolism reprogram macrophages to enhance their migratory and pro-tumor functions [2, 6].
• Therapeutic target: inhibiting positive regulators like ILT4 or osteopontin can boost anti-PD-L1 therapy and reduce tumor growth [1, 4].
• Role in neovascularization: M2 macrophage-derived migrasomes promote retinal neovascularization via TREM2, linking migration to angiogenesis.
• Inflammatory bone disease: IL6-PIEZO1 signaling enhances M1 macrophage migration in orthodontic root resorption.
• Glioma progression: GPR65 sensing lactate induces HMGB1 release from TAMs, promoting glioma progression.
• Biomarker potential: genes such as DOCK7 and CircABCA1 are associated with metastatic potential and could serve as prognostic markers [6, 7].
• CRISPR screening: high-throughput knockout screens can identify novel positive regulators of macrophage migration [1, 4].
• Drug discovery: small molecules targeting chemokine receptors or metabolic pathways can modulate macrophage migration [3, 5].
What Happens During positive regulation of macrophage migration?
Chemokine Sensing and Signal Initiation
In simple terms: Macrophages detect chemical signals that tell them where to move.
Positive regulation of macrophage migration begins when chemokines or other chemoattractants bind to G-protein-coupled receptors on the macrophage surface. For example, the CXCL12/CXCR4 axis is activated by IL6-dependent PIEZO1 signaling to promote M1 macrophage migration in orthodontic root resorption. Similarly, GPR65 senses tumor-derived lactate and triggers cAMP/PKA/CREB signaling, leading to HMGB1 release from tumor-associated macrophages and enhanced migration. These initial sensing events set the direction and intensity of macrophage movement.
Metabolic Reprogramming for Migration
In simple terms: Macrophages change how they use energy to fuel movement.
Migrating macrophages require substantial energy, and metabolic reprogramming is a key positive regulatory mechanism. Zeb1-induced glycolytic reprogramming is essential for macrophage polarization and migration in breast cancer. Additionally, CircABCA1 promotes clear cell renal cell carcinoma by reprogramming cholesterol metabolism and facilitating M2 macrophage polarization through IGF2BP3-mediated stabilization of SCARB1 mRNA. These metabolic shifts provide the ATP and biosynthetic precursors needed for cytoskeletal dynamics and membrane remodeling during migration.
Cytoskeletal Rearrangement and Motility Machinery
In simple terms: The cell's internal skeleton reorganizes to push the cell forward.
Downstream of chemokine and metabolic signals, macrophages undergo cytoskeletal rearrangement driven by Rho GTPases such as RAC1. Tumour-associated macrophage-derived DOCK7-enriched extracellular vesicles drive tumour metastasis in colorectal cancer via the RAC1/ABCA1 axis, demonstrating that DOCK7 promotes migratory machinery activation. Osteopontin also mediates glioblastoma-associated macrophage infiltration, likely through integrin signaling that converges on cytoskeletal effectors. These events enable the protrusion of lamellipodia and the retraction of the trailing edge, propelling the macrophage forward.
Extracellular Matrix Remodeling and Tissue Invasion
In simple terms: Macrophages clear a path through tissue to reach their target.
To migrate through tissues, macrophages must remodel the extracellular matrix. M2 macrophage-derived migrasomes mediate ischaemia-induced retinal neovascularization by targeting TREM2, indicating that migrasomes facilitate both migration and matrix interactions. In cancer, TAMs secrete factors that degrade matrix components, allowing infiltration into tumors such as glioblastoma and colorectal cancer [1, 7]. This remodeling step is a critical positive regulatory component of macrophage migration in pathological contexts.
Amplification by Cytokine and Checkpoint Signals
In simple terms: Other immune signals can boost or sustain macrophage movement.
Positive regulation of macrophage migration is often amplified by cytokines and immune checkpoint molecules. ILT4 inhibition prevents TAM- and dysfunctional T cell-mediated immunosuppression and enhances the efficacy of anti-PD-L1 therapy in NSCLC with EGFR activation, suggesting that ILT4 signaling modulates macrophage migration and function. IL6 promotes M1-mediated orthodontic root resorption via CXCL12/CXCR4, further illustrating how cytokines can enhance migratory responses. These amplification loops ensure robust macrophage recruitment during inflammation and cancer.
Key Genes Involved in GO:1905523 positive regulation of macrophage migration
The following genes and proteins have been experimentally linked to positive regulation of macrophage migration in the verified literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| SPP1 (Osteopontin) | Mediates glioblastoma-associated macrophage infiltration | Therapeutic target for glioblastoma; promotes TAM migration |
| ZEB1 | Induces glycolytic reprogramming for macrophage polarization | Essential for macrophage migration in breast cancer |
| GPR65 | Senses tumor-derived lactate; activates cAMP/PKA/CREB | Promotes HMGB1 release from TAMs and glioma progression |
| ILT4 (LILRB2) | Inhibits TAM- and T cell-mediated immunosuppression | Target for enhancing anti-PD-L1 therapy in NSCLC |
| PIEZO1 | Mechanosensitive ion channel activated by IL6 | Promotes M1 macrophage migration in orthodontic root resorption |
| CXCR4 | Chemokine receptor for CXCL12 | Mediates M1 macrophage migration in root resorption |
| IGF2BP3 | Stabilizes SCARB1 mRNA | Facilitates M2 macrophage polarization in ccRCC |
| SCARB1 | Cholesterol metabolism regulator | Reprogramming cholesterol metabolism for M2 polarization |
| DOCK7 | RAC1 guanine nucleotide exchange factor | Enriched in TAM-derived EVs; drives colorectal cancer metastasis |
| RAC1 | Rho GTPase regulating cytoskeleton | Mediates TAM EV-induced migration and metastasis |
| ABCA1 | Cholesterol efflux transporter | Involved in RAC1/ABCA1 axis in colorectal cancer |
| TREM2 | Lipid-sensing receptor on macrophages | Target of M2 macrophage-derived migrasomes in retinal neovascularization |
| HMGB1 | Nuclear protein released by TAMs | Promotes glioma progression downstream of GPR65 |
| IL6 | Pro-inflammatory cytokine | Activates PIEZO1 to promote M1 macrophage migration |
| CXCL12 | Chemokine ligand for CXCR4 | Recruits M1 macrophages in root resorption |
| cAMP/PKA/CREB | Signaling pathway downstream of GPR65 | Induces HMGB1 release from TAMs |
| CircABCA1 | Circular RNA regulating cholesterol metabolism | Promotes ccRCC via M2 macrophage polarization |
How Is positive regulation of macrophage migration Regulated?
Positive regulation of macrophage migration is controlled at multiple levels. At the receptor level, GPR65 senses lactate and activates cAMP/PKA/CREB signaling to induce HMGB1 release. Cytokine signaling through IL6 activates PIEZO1, which in turn promotes CXCL12/CXCR4-mediated migration. Metabolic regulation occurs through Zeb1-induced glycolysis and CircABCA1-mediated cholesterol metabolism. At the cytoskeletal level, DOCK7 activates RAC1 to drive migratory machinery. Immune checkpoint molecules such as ILT4 can modulate the overall migratory response. These layers of regulation ensure that macrophage migration is tightly controlled and can be rapidly amplified during inflammation or tumor progression.
positive regulation of macrophage migration and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| SPP1 (Osteopontin) | Glioblastoma | Knockout mice or glioblastoma cell lines with SPP1 KO |
| ZEB1 | Breast cancer | Zeb1 conditional knockout in mammary tumor models |
| GPR65 | Glioma | GPR65 knockout glioma cells or TAM-specific KO |
| ILT4 (LILRB2) | NSCLC with EGFR activation | ILT4 knockout or overexpression in NSCLC models |
| PIEZO1 | Orthodontic root resorption | Piezo1 knockout mice or conditional KO in macrophages |
| CircABCA1 | Clear cell renal cell carcinoma | CircABCA1 knockdown or overexpression in ccRCC cells |
| DOCK7 | Colorectal cancer metastasis | DOCK7 knockout in TAMs or colorectal cancer cells |
| TREM2 | Retinal neovascularization | TREM2 knockout mice in oxygen-induced retinopathy |
Cancer Progression and Metastasis
Positive regulation of macrophage migration is a hallmark of tumor progression. Osteopontin mediates glioblastoma-associated macrophage infiltration, and targeting it reduces tumor growth. In breast cancer, Zeb1-induced glycolytic reprogramming is essential for macrophage polarization and migration. GPR65 sensing of tumor-derived lactate promotes HMGB1 release from TAMs, driving glioma progression. Colorectal cancer metastasis is driven by TAM-derived DOCK7-enriched extracellular vesicles via the RAC1/ABCA1 axis. In clear cell renal cell carcinoma, CircABCA1 promotes M2 macrophage polarization through cholesterol metabolism reprogramming. These findings underscore the therapeutic potential of targeting positive regulators of macrophage migration in cancer.
Inflammatory and Bone Diseases
In orthodontic root resorption, IL6-dependent PIEZO1 activation promotes M1 macrophage migration via CXCL12/CXCR4, contributing to inflammatory bone destruction. This highlights how positive regulation of macrophage migration can drive pathological inflammation in bone and dental tissues. Modulating this process could offer new strategies for treating inflammatory bone diseases.
Retinal Neovascularization
M2 macrophage-derived migrasomes mediate ischaemia-induced retinal neovascularization by targeting TREM2. This demonstrates that positive regulation of macrophage migration and subsequent migrasome release contribute to aberrant angiogenesis in the eye, suggesting TREM2 as a potential therapeutic target for retinal neovascular diseases.
Immunotherapy Resistance
ILT4 inhibition prevents TAM- and dysfunctional T cell-mediated immunosuppression and enhances the efficacy of anti-PD-L1 therapy in NSCLC with EGFR activation. This links positive regulation of macrophage migration to immunotherapy resistance, as TAM infiltration and migration can create an immunosuppressive tumor microenvironment. Targeting migratory pathways may improve responses to immune checkpoint inhibitors.
From positive regulation of macrophage migration-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does gene X positively regulate macrophage migration? | CRISPR knockout of gene X in macrophage cell lines (e.g., RAW264.7, THP-1) followed by transwell migration assay [1, 5] |
| Does a specific point mutation in gene X alter migratory capacity? | CRISPR point mutation knock-in in primary macrophages or iPSC-derived macrophages [3, 4] |
| Does overexpression of gene X enhance macrophage migration? | Lentiviral overexpression of gene X in macrophages followed by chemotaxis assays [2, 6] |
| Does a tagged version of gene X localize to migratory structures? | CRISPR knock-in of fluorescent tag (e.g., GFP) at endogenous locus |
| What is the role of gene X in tumor-associated macrophage infiltration? | Bone marrow chimera or conditional knockout mice in tumor models [1, 7] |
| Can CRISPR screening identify novel regulators of macrophage migration? | Genome-wide CRISPR knockout library in macrophage cell lines under chemotactic selection [4, 8] |
How to Study the positive regulation of macrophage migration Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Transwell migration assay | Number of cells migrating through a membrane | Quantify macrophage chemotaxis in vitro [1, 5] |
| Live-cell imaging | Real-time cell movement and morphology | Track cytoskeletal dynamics and migrasome release [7, 8] |
| CRISPR knockout screen | Genes required for migration | Identify novel positive regulators [4, 6] |
| RNA-seq | Transcriptional changes during migration | Discover pathways upregulated in migrating macrophages [2, 3] |
| Proteomics | Protein expression and modifications | Identify signaling effectors and biomarkers |
| Metabolic flux analysis | Glycolysis, oxidative phosphorylation | Assess metabolic reprogramming [2, 6] |
| Flow cytometry | Macrophage polarization markers | Correlate migration with M1/M2 phenotype [4, 8] |
| In vivo intravital imaging | Macrophage migration in living tissue | Study TAM infiltration in tumors [1, 7] |
Transwell Migration Assays
Transwell assays are the gold standard for measuring macrophage migration in vitro. Macrophages are placed in the upper chamber and chemoattractants in the lower chamber; migrated cells are quantified. This method has been used to demonstrate that osteopontin promotes glioblastoma-associated macrophage infiltration and that IL6-PIEZO1 signaling enhances M1 macrophage migration.
Live-Cell Imaging and Chemotaxis Analysis
Live-cell imaging allows real-time tracking of macrophage movement in response to chemokine gradients. This technique can visualize cytoskeletal dynamics and has been applied to study DOCK7-enriched extracellular vesicle-driven migration in colorectal cancer. It is also useful for assessing migrasome formation in retinal neovascularization.
CRISPR Screening and Functional Genomics
Genome-wide CRISPR knockout or activation screens can identify novel positive regulators of macrophage migration. By selecting for cells that migrate more or less efficiently, researchers can uncover genes such as those involved in metabolic reprogramming [2, 6] or checkpoint signaling. These screens are powerful for unbiased discovery.
Metabolic and Proteomic Profiling
Metabolic assays (e.g., Seahorse) and proteomics can reveal how metabolic reprogramming supports macrophage migration. Zeb1-induced glycolysis and CircABCA1-mediated cholesterol metabolism were identified using such approaches. Proteomics can also identify post-translational modifications and protein-protein interactions that regulate migration.
How CRISPR Can Be Used to Study GO:1905523 positive regulation of macrophage migration
Knockout
CRISPR knockout of candidate genes in macrophage cell lines or primary macrophages is used to determine whether a gene is required for positive regulation of migration. For example, knocking out SPP1 or PIEZO1 reduces macrophage infiltration in glioblastoma and root resorption models, respectively [1, 5]. Knockout models are essential for loss-of-function studies.
Point Mutation
CRISPR point mutation knock-in allows researchers to introduce specific amino acid changes to test the function of particular residues or domains. This is useful for dissecting signaling pathways, such as mutations in GPR65 that affect lactate sensing or in ILT4 that alter checkpoint function. Point mutations can reveal mechanistic details that knockout cannot.
Knock-in
CRISPR knock-in of reporter tags (e.g., GFP, luciferase) or epitope tags at endogenous loci enables visualization and tracking of proteins during macrophage migration. Tagged DOCK7 or TREM2 knock-in models can be used to study protein localization and dynamics in real time [7, 8]. Knock-in of conditional alleles (e.g., loxP) also allows tissue-specific deletion.
Overexpression
CRISPR activation (CRISPRa) or lentiviral overexpression is used to test whether increasing the level of a gene enhances macrophage migration. Overexpression of Zeb1 or CircABCA1 promotes migratory and pro-tumor phenotypes in breast cancer and ccRCC models [2, 6]. Overexpression studies complement knockout approaches to establish sufficiency.
How EDITGENE Supports positive regulation of macrophage migration Research
Researchers studying positive regulation of macrophage migration-related genes often need to determine whether a candidate gene is causally involved in enhancing macrophage motility. EDITGENE provides a comprehensive suite of CRISPR-based services to accelerate this research, from gene knockout to precise point mutations, knock-ins, and overexpression, as well as high-throughput library screening and bioinformatics analysis.
Contact EDITGENE today to design your custom CRISPR model for positive regulation of macrophage migration research.
Frequently Asked Questions About positive regulation of macrophage migration
What is GO:1905523 positive regulation of macrophage migration?
GO:1905523 is a Gene Ontology biological process term defined as any process that activates or increases the frequency, rate, or extent of macrophage migration. It encompasses molecular signals and cellular changes that enhance macrophage movement [1, 5].
What genes are involved in positive regulation of macrophage migration?
Key genes include SPP1 (osteopontin), ZEB1, GPR65, ILT4, PIEZO1, CXCR4, DOCK7, RAC1, ABCA1, TREM2, and CircABCA1, among others [1, 2, 3, 4, 5, 6, 7, 8].
How is macrophage migration positively regulated in cancer?
In cancer, tumor-derived factors such as osteopontin, lactate, and extracellular vesicles activate signaling pathways (e.g., GPR65-cAMP/PKA/CREB, DOCK7-RAC1) that enhance macrophage migration and tumor infiltration [1, 3, 7].
What experimental models are used to study positive regulation of macrophage migration?
Common models include transwell migration assays, live-cell imaging, CRISPR knockout/knock-in mice, and genome-wide CRISPR screens in macrophage cell lines [1, 4, 5, 7].
How does metabolic reprogramming affect macrophage migration?
Metabolic shifts such as increased glycolysis (Zeb1-induced) and altered cholesterol metabolism (CircABCA1/SCARB1) provide energy and biosynthetic precursors that fuel macrophage migration and polarization [2, 6].
What is the role of GPR65 in macrophage migration?
GPR65 senses tumor-derived lactate and activates cAMP/PKA/CREB signaling, leading to HMGB1 release from tumor-associated macrophages and promoting glioma progression.
Can CRISPR be used to study positive regulation of macrophage migration?
Yes, CRISPR knockout, point mutation, knock-in, and overexpression models allow precise dissection of genes that positively regulate macrophage migration [1, 4, 5, 7].
What diseases are associated with dysregulated macrophage migration?
Diseases include glioblastoma, breast cancer, colorectal cancer, clear cell renal cell carcinoma, NSCLC, orthodontic root resorption, and retinal neovascularization [1, 2, 3, 4, 5, 6, 7, 8].
How does IL6 promote macrophage migration?
IL6 activates PIEZO1, which in turn promotes M1 macrophage migration via the CXCL12/CXCR4 axis in orthodontic root resorption.
What is the therapeutic potential of targeting positive regulators of macrophage migration?
Targeting regulators like osteopontin, ILT4, or TREM2 can reduce tumor progression, enhance immunotherapy, and treat neovascular diseases [1, 4, 8].
Conclusion
GO:1905523 (positive regulation of macrophage migration) is a critical biological process that governs macrophage recruitment in inflammation, tissue repair, and cancer. The verified literature highlights diverse molecular mechanisms, from chemokine sensing and metabolic reprogramming to cytoskeletal rearrangement and extracellular vesicle signaling [1, 2, 3, 5, 6, 7]. Dysregulation of this process contributes to tumor progression, immunotherapy resistance, and neovascular diseases, making it an attractive therapeutic target [1, 4, 8]. Researchers can leverage CRISPR-based models, including knockout, point mutation, knock-in, and overexpression, to dissect the causal roles of specific genes in macrophage migration. EDITGENE offers end-to-end services to support these studies, from custom cell line generation to high-throughput screening and bioinformatics, empowering discoveries that may translate into novel treatments for cancer and inflammatory diseases.
References
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- 3. Yan C et al.. 2024. GPR65 sensing tumor-derived lactate induces HMGB1 release from TAM via the cAMP/PKA/CREB pathway to promote glioma progression.. J Exp Clin Cancer Res 43(1):105 PMID: 38576043
- 4. Chen X et al.. 2021. ILT4 inhibition prevents TAM- and dysfunctional T cell-mediated immunosuppression and enhances the efficacy of anti-PD-L1 therapy in NSCLC with EGFR activation.. Theranostics 11(7):3392-3416 PMID: 33537094
- 5. Zhang ZH et al.. 2025. IL6-Dependent PIEZO1 Activation Promotes M1-Mediated Orthodontic Root Resorption via CXCL12/CXCR4.. J Dent Res 104(7):763-773 PMID: 40077814
- 6. Ning H et al.. 2025. CircABCA1 promotes ccRCC by reprogramming cholesterol metabolism and facilitating M2 macrophage polarization through IGF2BP3-mediated stabilization of SCARB1 mRNA.. Mol Cancer 24(1):199 PMID: 40684174
- 7. Chen W et al.. 2024. Tumour-associated macrophage-derived DOCK7-enriched extracellular vesicles drive tumour metastasis in colorectal cancer via the RAC1/ABCA1 axis.. Clin Transl Med 14(2):e1591 PMID: 38385857
- 8. Li B et al.. 2025. M2 Macrophage-Derived Migrasomes Mediate Ischaemia-Induced Retinal Neovascularization by Targeting TREM2.. J Extracell Vesicles 14(11):e70180 PMID: 41170761
