# NIH grant: Biophysical Regulation of Macrophages Through Engineered Material Platforms (1R35GM166254-01) — retained record

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[original source ↗](https://reporter.nih.gov/project-details/1R35GM166254-01)

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NIH grant 1R35GM166254-01: Biophysical Regulation of Macrophages Through Engineered Material Platforms
Institute: {'code': 'GM', 'abbreviation': 'NIGMS', 'name': 'National Institute of General Medical Sciences', 'admin_org_id': '12500024', 'admin_funding_url': ''}. PI: Ramkumar  Tiruvannamalai Annamalai. Award: $432844.
Start: 2026-07-10T00:00:00.
PROJECT ABSTRACT/SUMMARY
 Macrophages, vital regulators of inflammation and tissue repair, are profoundly influenced by mechanical
cues in their microenvironments, such as stiffness, spatial architecture, and dynamic forces. These cues are
disrupted in aging, injury, and diseases like fibrosis and cancer, driving maladaptive immune responses. While
stiffness has been studied, the independent roles of geometry, viscoelasticity, and intracellular force in shaping
macrophage states remain unexplored. Current models oversimplify these dynamics and fail to capture the
translational complexity of living tissues.
 To close this gap, we will develop and apply dynamic, cell-instructive biomaterials that emulate native
mechanics while benchmarking their outputs against macrophage states from in vivo injury and fibrotic datasets.
Our program integrates three innovations: (1) Curvature platforms spanning fibril- to tissue-scale geometries to
dissect cytoskeletal partitioning and MRTF-A-driven transcription; (2) Viscoelastic hydrogels under cyclic loading
to identify mechanical “tipping points” between regenerative versus fibrotic polarization; and (3) Intracellular
nanomaterial actuation to test whether direct cytoskeletal force alone reprograms inflammatory and fibrotic
transcription. Predefined success metrics and alternative approaches will ensure rigor and reproducibility.
 These platforms will serve dual roles: (i) as foundational tools to reveal mechanoimmunology principles,
and (ii) as translational blueprints for “mechanotherapies.” For example, curvature-tuned scaffolds may suppress
tissue fibrosis, viscoelastic implants may accelerate wound repair, and intracellular force actuators may silence
chronic inflammation in arthritis. By merging engineering with immunology and grounding models in physiologic
benchmarks, this research establishes macrophages as sentinels of mechanical dysfunction and opens new
therapeutic avenues for fibrosis, chronic wounds, and cancer.
```



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