Cardiovascular disease (CVD) is no longer viewed as a purely hemodynamic problem—it is a systems-level inflammatory condition where macrophages act as "decision-makers" across initiation, progression, destabilization, and repair. From foam-cell formation in atherosclerosis to post-infarction remodeling, macrophages integrate lipid cues, mechanical stress, hypoxia, damage-associated signals, and cytokine networks to shape tissue outcomes. Importantly, cardiovascular macrophages rarely fit into a simple M1/M2 box; instead, they occupy a spectrum of activation states driven by tissue niche, metabolic programming, and time after injury.

Creative Biolabs provides a disease-relevant, modular suite of macrophage-centered CVD study services.

Macrophage Biology in Cardiovascular Disease

Macrophages are innate immune cells that reside and accumulate in healthy and damaged hearts, and those cells play a pivotal role during both myocardial tissue damage and repair. Macrophage accumulation is not only a characteristic of PAH but also a key component of pulmonary artery remodeling associated with PAH. During myocardial infarction (MI), AS and stroke, monocytes are supplied by medullary and extramedullary hematopoiesis in bone marrow and spleen. Monocytes infiltrate diseased tissues, differentiate into macrophages and proliferate locally. Angiogenesis and healing of the infarcted heart after damage are promoted by cardiac macrophages derived from the early embryonic cells. Arterial macrophages in AS persist. In AS, macrophage uptake of oxidized lipoprotein exceeds the formation of cholesterol, leading to the accumulation of cholesterol esters, eventual development of foam cells, and plaque development, leading to stroke finally. Perivascular macrophages may play a role in hypertension, specifically the neurological symptoms and cognitive impairment associated with chronic hypertension.

Fig.1 Macrophages orchestrate the regenerative process post-MI.^1,2

Macrophages are composed of two main phenotypes: M1 and M2 macrophage. In AS, M1 macrophages are correlated to plaque vulnerability. Generally, M2 macrophages can activate vascular remodeling and M1 macrophages increase perivascular inflammation, vascular permeability, and fibrosis. Therefore, the presence of M2 macrophages is associated with the progression of PAH and the proliferation of pulmonary artery smooth muscle cells. M1-polarized macrophages are typically found during the early stage of myocardial infarction (MI) leading to acute pro-inflammatory and immune polarization reactions. M1 macrophages can aggravate insult after MI and increase the occurrence of ventricular tachycardia which contributes to ventricular arrhythmias. While M2-polarized macrophages are present during the terminal stages of MI to increase myocardial tissue repair. M2 macrophages with anti-inflammatory and antifibrosis effects reduce rapid morbidity from ventricular tachycardia after MI.

To support our clients' specific objectives of macrophage development projects, Creative Biolabs is proud to provide the most comprehensive and professional services list. For more information on the role of macrophage in cardiovascular diseases, please click on the links below.

• Macrophages in Atherosclerosis (AS)
• Macrophages in Pulmonary arterial Hypertension (PAH)
• Macrophages in Cardiac Diseases

Our Cardiovascular Macrophage Services

Creative Biolabs offers a comprehensive suite of services tailored to the unique requirements of cardiovascular research. We bridge the gap between basic immunology and clinical cardiology through disease-specific models and multi-omic readouts.

Cardiovascular-Specific Macrophage Models

• Primary Human & Murine Models: Isolation of Cardiac Resident Macrophages (CRMs) and Bone Marrow-Derived Macrophages (BMDMs).
• Atherosclerosis-Mimetic Models: Induction of "Foam Cells" using oxidized LDL (oxLDL) or acetylated LDL (acLDL) in primary or THP-1 macrophages.
• Hypoxia/Reoxygenation (H/R) Models: Simulating myocardial ischemia-reperfusion injury in vitro.
• Hemodynamic Stress Models: Evaluating macrophage response to shear stress and cyclic stretch in co-culture with endothelial cells.

Advanced Phenotyping & Characterization

• Multi-Parametric Flow Cytometry: Identification of subsets and markers like MerTK, CD163, and CD206.
• Efferocytosis Assays: Quantitative analysis of macrophage capacity to clear apoptotic cardiomyocytes or vascular smooth muscle cells (VSMCs).
• Metabolic Profiling: Assessing the glycolytic shift in inflammatory macrophages vs. oxidative phosphorylation in resolving macrophages.
• Spatial Transcriptomics & Imaging: Mapping macrophage niches within the atherosclerotic plaque or the infarct border zone.

Functional Assessment in CVD Context

• Pro-inflammatory Signaling: NLRP3 inflammasome activation and IL-1β/IL-18 secretion assays.
• Angiogenesis & Fibrosis Assays: Evaluating how macrophage-conditioned media influences endothelial tube formation or fibroblast-to-myofibroblast transformation.
• Chemotaxis & Recruitment: Measuring monocyte migration toward CVD-relevant chemokines (e.g., CCL2, CX3CL1).

Specific Disease Modules

Workflow

• Project Consultation: Define the specific CVD indication (e.g., stable vs. unstable plaque) and primary endpoints.
• Model Customization: Selection of cell sources (human PBMC, mouse BMDM) and CVD-specific stimuli (oxLDL, hypoxia, Ang II).
• Experimental Execution: Polarization and treatment with candidate compounds (small molecules, biologics, or RNAi).
• Data Acquisition: High-content imaging, flow cytometry, ELISA, or RNA-seq.
• Integrated Analysis: Professional data interpretation, pathway mapping, and publication-ready reporting.

Strategies of Targeting Macrophages in CVD

• Depletion or inactivation of macrophages is a potential route to reduce inflammation and delay the progression of CVD. Some reports demonstrated that the delivery of clodronate by liposomes eliminated macrophages. Blockage of macrophage-derived cytokines is another potential approach to remove CD68+ macrophages and retard PAH development.
• Reprogramming of macrophages toward M2 phenotypes is one potential strategy to treat AS and cardiac diseases such as myocarditis. While inhibition of macrophages by reduced expression of interleukin 21 (IL-21) can ameliorate PAH.
• Reducing the blood-derived monocyte recruitment and infiltration is beneficial to limit inflammation or atherosclerotic plaque progression after PAH, AS, MI and myocardial fibrosis (MF). Targeted delivery of anti-oxidative agents to macrophages to inhibit the secretion of pro-inflammatory factors, such as reactive oxygen species (ROS), tumor necrosis factor (TNFα), IL-1β, and monocyte chemoattractant protein-1 (MCP-1), is a well-demonstrated strategy to induce regression of AS.

Creative Biolabs' Macrophage Research Solutions for Cardiovascular Disease Studies

Below is a practical mapping of study goals to service modules commonly used in cardiovascular macrophage programs.

Why Choose Creative Biolabs

• CVD-relevant modularity: start lean, scale depth without re-building the platform
• High-quality cell sources and QC: consistent viability/purity expectations for reproducible datasets
• Multi-dimensional detection capability: phenotype + function + mechanism in one coordinated plan
• Scientist-led interpretation: outputs designed to support confident project decisions, not just raw readouts

Related Products

Curated, assay-ready reagents and tools can be aligned to cardiovascular macrophage workflows, including:

Scientific Resources

Q & A

Q: Can you tailor the model to our specific CVD indication—atherosclerosis vs. myocardial infarction vs. heart failure vs. vascular remodeling?

A: Yes. We build indication-aligned modules rather than a one-size-fits-all macrophage panel. For atherosclerosis programs, we emphasize lipid loading/foam-cell formation, cholesterol handling, inflammasome-linked stress, and efferocytosis under plaque-like conditions.

Q: Which macrophage sources do you offer, and how should we choose between primary human cells and cell lines?

A: We support human primary monocyte-derived macrophages, common research cell-line platforms (e.g., THP-1-derived macrophages), and relevant preclinical macrophage sources (e.g., BMDMs). Primary human macrophages are best for translational relevance and donor-to-donor robustness testing, while cell lines are ideal for high-throughput screening, reproducibility, and early rank-ordering. Many clients take a hybrid approach: screen in a standardized platform first, then confirm the top candidates in primary human macrophages (optionally across multiple donors).

Q: Can you capture time-dependent macrophage transitions rather than a single endpoint?

A: We often propose a time-course design with carefully selected sampling points that reflect early inflammatory phases and later reparative shifts. We combine phenotyping with functional outputs (phagocytosis/efferocytosis, secretome profiling, migration) and optionally add macrophage–fibroblast or macrophage–endothelial co-culture modules to translate macrophage transitions into remodeling-relevant outputs.

Q: What does the final deliverable package include?

A: Deliverables commonly include raw data files, QC documentation, summarized results tables, and an interpretation-focused report that maps outputs to your success criteria.

Q: How flexible is the scope?

A: Very flexible. Many teams begin with a tight screening panel, then pivot toward deeper mechanism or co-culture modules once the data clarifies the strongest axis. Because our service is modular, we can expand readouts, add timepoints, include donor replication, or test additional stimuli without rebuilding the entire workflow from scratch.

References

1. de Couto, Geoffrey. "Macrophages in cardiac repair: environmental cues and therapeutic strategies." Experimental & molecular medicine 51.12 (2019): 1-10. https://doi.org/10.1038/s12276-019-0269-4
2. Distributed under Open Access license CC BY 4.0, without modification.