Atherosclerosis – Preclinical Models of Chronic Vascular Inflammation

Atherosclerosis is a chronic inflammatory disease of the arterial wall and the primary pathological process underlying cardiovascular diseases such as myocardial infarction, stroke, and peripheral artery disease. It is characterized by lipid accumulation, immune cell infiltration, plaque formation, and endothelial dysfunction.

At Redoxis, we offer in vivo models of atherosclerosis in genetically modified mice that recapitulate key aspects of human disease. These models are suitable for evaluating anti-inflammatory, lipid-lowering, and plaque-stabilizing therapies, as well as immunomodulators that target key immune components in vascular inflammation.

The ApoE-deficient (ApoE⁻/⁻) mouse is the most commonly used genetic model for studying atherosclerosis. ApoE⁻/⁻ mice spontaneously develop hypercholesterolemia and atherosclerotic lesions, which are accelerated by feeding a high-fat or Western-type diet.

Plaques form primarily in the aortic root and arch, resembling early- to mid-stage human atherosclerosis. Inflammation, lipid accumulation, foam cell formation, and necrotic core development can be quantified histologically and by immunohistochemistry.

Key Features:

  • Genetic model of spontaneous atherosclerosis
  • Accelerated disease on high-fat diet
  • Lesions in aortic root, arch, and carotid arteries
  • Involves innate and adaptive immune responses
  • Suitable for testing anti-inflammatory, lipid-lowering, or immune-targeted therapies
  • Compatible with histology, lipid profiling, and flow cytometry of immune cells in aorta and lymphoid organs

The LDL receptor-deficient (LDLr⁻/⁻) mouse develops atherosclerosis upon high-fat or high-cholesterol diet and is often used to model diet-induced atherogenesis with greater sensitivity to dietary lipid changes compared to ApoE⁻/⁻ mice.

This model is relevant for studying lipid metabolism, lipoprotein clearance, and the effects of dietary or pharmacological interventions.

Key Features:

  • Diet-induced atherosclerosis in genetically modified mice
  • Sensitive to changes in dietary cholesterol and lipid metabolism
  • Useful for evaluating lipid-lowering agents (e.g., statins, PCSK9 inhibitors)
  • Supports analysis of lesion development and inflammatory infiltration

Readouts and Capabilities

Redoxis offers a range of endpoints and analyses for atherosclerosis studies, including:

  • Histological analysis of aortic root and en face aortic plaque area
  • Immunohistochemistry for macrophages, T cells, smooth muscle cells, and collagen
  • Plasma lipid profiling (cholesterol, triglycerides, lipoprotein fractions)
  • Flow cytometry of aortic and lymphoid immune cells
  • Cytokine analysis (e.g., IL-6, TNF-α, IL-1β) in serum and tissues
  • Gene expression profiling from aorta or plaques

Redoxis’ atherosclerosis models offer translational relevance for the development of novel therapies targeting chronic vascular inflammation, immune regulation, and plaque stabilization. Contact us to discuss study design, model selection, or integration with systemic inflammation or autoimmunity models.

The bleomycin model is the most commonly used preclinical model for pulmonary fibrosis. It is induced by intratracheal, intranasal, or systemic (e.g., intraperitoneal) administration of bleomycin in mice, leading to acute lung injury followed by chronic fibrotic remodeling.

Fibrosis typically develops within 1–2 weeks, with severity and kinetics depending on dose and route of administration. Histologically, the model features alveolar damage, immune cell infiltration, and progressive collagen deposition.

Key Features:

  • Induced by bleomycin (intratracheal, intranasal, or systemic)
  • Biphasic progression: early inflammation followed by fibrosis
  • Collagen accumulation measurable by histology or biochemical assays (e.g., hydroxyproline)
  • Suitable for evaluating anti-fibrotic and anti-inflammatory therapies
  • Compatible with lung histology, gene/protein expression, BALF analysis, and cytokine profiling

Assay Capabilities and Readouts

Redoxis provides a full suite of analytical endpoints for lung fibrosis studies, including:

  • Histopathology and immunohistochemistry (e.g., collagen I/III, α-SMA, fibronectin)
  • Hydroxyproline assay for quantitative collagen content
  • BALF analysis for inflammatory cell counts and cytokines
  • qPCR, ELISA, and Luminex for fibrosis- and inflammation-associated markers
  • Flow cytometry of lung-resident and infiltrating immune cells
  • Ex vivo lung cell stimulation assays to evaluate immune modulation

Our lung fibrosis model provides a translational platform for preclinical testing of novel compounds aimed at modifying fibrotic progression, reducing inflammation, or preserving lung function. Contact us for detailed protocols or to tailor a study to your compound’s mechanism of action.

Contact us

Inquiries? Questions?

Nina Woodworth

COO