Atherosclerosis (AS) is not simply a lipid-storage disorder—it is a chronic, immune-driven remodeling process in the arterial wall. From the earliest fatty streak to advanced, rupture-prone plaques, macrophages orchestrate lesion initiation, progression, and destabilization through lipid uptake, inflammatory signaling, efferocytosis failure, and crosstalk with endothelial cells (ECs), smooth muscle cells (VSMCs), and adaptive immune populations. At Creative Biolabs, we build disease-relevant, modular macrophage assays and models for atherosclerosis studies.

Macrophages at the Core of Atherosclerotic Inflammation

The key initiating step of AS is the subendothelial accumulation of lipoproteins to induce the activation of the overlying endothelium. Subsequently, monocytes are recruited to enter the subendothelial cell space and locate in the lesion site. Monocytes further differentiate into macrophages to actively scavenge normal and modified lipoproteins and become foam cells. Foam cells accumulate in the intima and go through apoptosis by cytokines. These foam cells persist in plaques to promote AS development. In these advanced plaques, macrophages continue to be major contributors to the inflammatory response. Dying macrophages release their lipid contents and tissue factors, which leads to forming a prothrombotic necrotic core triggering rupture and thrombosis finally.

Fig.1 Roles of macrophages in different stages of atherosclerosis progression.^1,2

In AS plaques, macrophages adapt their phenotype to different stimuli. From a functional point of view, Mhem, M(Hb), and M2 macrophages prevent forming foam cells and play a crucial role in iron handling. M1 macrophages display a pro-inflammatory profile and are found in rupture-prone lesions which suggest that these macrophages are associated with plaque vulnerability. Mox macrophages exhibit reduced phagocytic capacity and express anti-oxidant genes. M4 macrophages also display reduced phagocytic capacity and a pro-inflammatory profile.

Fig.2 Macrophage subsets in the atherosclerotic lesion.^1,2

What We Offer

Creative Biolabs provides a comprehensive macrophage services for atherosclerosis study solution centered on disease relevance, mechanism-driven design, and data clarity. You can run a focused foam cell module—or integrate a full "plaque-like" program that spans phenotype, function, and vascular crosstalk.

• Disease-relevant model library (built for AS questions) - We design macrophage models around your indication stage, hypothesis, and translational plan.
• Physiologic plaque cues and controllable interventions - Atherosclerosis macrophage behavior is stimulus-dependent; we therefore offer "plug-and-play" inputs to mimic plaque context and to evaluate your test articles under the right conditions.
• Multi-modal readouts designed for decision-making - Atherosclerosis macrophage research becomes actionable when the readouts are aligned to the "axes" that matter.

Below is a practical view of how most atherosclerosis macrophage programs are structured.

Creative Biolabs' Macrophage Research Solutions for Atherosclerosis Studies

Creative Biolabs supports macrophage-AS projects with a flexible suite of services—assembled into a study plan that matches your endpoints and timelines.

• Macrophage Isolation and Culture Service
  High-quality primary macrophage preparation from PBMCs, bone marrow, or tissue-appropriate sources.
• Macrophage Polarization Assay Service
  Controlled polarization and state conditioning, expanded to plaque-relevant stimuli beyond classical M1/M2 where needed.
• Macrophage Phenotype Identification Service
  Multi-marker phenotyping strategies to quantify macrophage states, including foam cell–associated signatures.
• Macrophage Functional Assays
  Phagocytosis and efferocytosis modules, migration assays, antigen presentation endpoints (when immune crosstalk is in scope), and additional function panels aligned to your MoA.
• Cytokine Expression Profiling
  Quantitative cytokine/chemokine outputs that connect phenotype shifts to immune impact.
• Macrophage Reprogramming Service
  Mechanism-forward reprogramming evaluations (including microRNA-, nanoparticle-, or regulatory-network-centered hypotheses).
• Macrophage-targeted Drug Delivery System Development
  Macrophage-targeting strategies for study-stage delivery concepts (nanoparticles/liposomes/dendrimers).

Service Workflow

Therapies of Targeting Macrophages in AS

• Reducing macrophage recruitment to atherosclerotic plaques by inhibition of chemokine receptors, such as chemokine (C-X3-C motif) receptor 1 (CX3CR1), chemokine receptor 2 (CCR2), and CCR5.
• Reprogramming of macrophages to an anti-inflammatory M2 phenotype.
• Maintaining levels of efferocytosis, such as reducing inflammation (in the case of IL-10 and liver X receptor (LXR) agonists) or promoting cholesterol efflux (in the case of LXR agonists, increasing autophagy or ATP-binding cassette transporter A1 (ABCA1) and ATP-binding cassette, sub-family G member 1 (ABCG1) expression levels by inhibiting the miR-33).
• Novel drug delivery systems selectively modify macrophages including inducing cell apoptosis, inhibiting cell proliferation, and introducing anti-inflammatory agents.

The discovery of different macrophage phenotypes provides an opportunity to study the relationship between macrophage phenotypes and diseases. Based on a Macrophage Therapeutics Development Platform, Creative Biolabs is offering the most comprehensive services for macrophage development projects. We are committed to providing customized professional and efficient solutions to support your projects.

Why Teams Choose Creative Biolabs for AS Macrophage Studies?

• Study designs built around plaque biology, not generic macrophage stimulation
• Modular workflows that scale from hypothesis testing to candidate ranking
• Multi-dimensional endpoints that connect lipid handling, inflammation, and efferocytosis into one interpretable story
• Strong QC and SOP discipline to keep longitudinal datasets comparable
• Report-ready outputs designed for internal decisions and external communication

Related Products

Below is an example of macrophage-related products that can support atherosclerosis research. For a full, up-to-date list, please refer to our product catalog.

Scientific Resources

Q & A

Q: Can you design atherosclerosis macrophage studies that go beyond the M1/M2 framework?

A: Yes. Atherosclerotic plaques contain macrophage states shaped by lipid overload, oxidative stress, heme/iron cues, and cytokine gradients. We design phenotype mapping and functional readouts that capture foam cell programs, inflammatory signaling, and efferocytosis competence—so your dataset reflects plaque biology rather than oversimplified polarization labels.

Q: Can you test my nanoparticle/liposome concept in plaque-like macrophage conditions?

A: Yes. We evaluate uptake and intracellular routing under lipid-loaded or inflammatory states, monitor activation liabilities (cytokines/inflammasome proxies), and quantify functional consequences such as efferocytosis and lipid handling. This helps distinguish "good uptake" from "useful biology."

Q: What macrophage sources do you recommend for atherosclerosis studies—primary cells or cell lines?

A: It depends on your phase. For early screening and optimization, scalable cell models are efficient. For mechanistic validation and translational confidence, human primary monocyte-derived macrophages are often preferred. Many projects run both: a screening tier followed by a confirmatory tier in primary macrophages to de-risk interpretation.

Q: What does a typical timeline look like for a macrophage-AS program?

A: Timelines depend on model complexity, number of conditions, and readouts. A focused foam cell module is generally faster, while integrated plaque-like programs require additional time for conditioning, co-culture/3D modules, and multi-omics analysis. We can structure phased deliverables so you receive early signals while deeper datasets are in progress.

Discuss your atherosclerosis indication stage, macrophage hypothesis, and decision timeline with our scientists. Creative Biolabs will tailor a macrophage-AS study plan that delivers clear, comparable data—built for confident go/no-go decisions.

All products and services are For Research Use Only and not for clinical applications.

References

1. Xu, Hailin, et al. "Vascular macrophages in atherosclerosis." Journal of immunology research 2019.1 (2019): 4354786. https://doi.org/10.1155/2019/4354786
2. Distributed under Open Access license CC BY 4.0, without modification.