# Polymeric Fibrous Materials for Procoagulant and Anticoagulant Applications: A Review of Molecular Blood–Material Mechanisms and Strategies

**Authors:** Marcin H. Kudzin, Monika Sikora, Zdzisława Mrozińska, Jerzy J. Chruściel

PMC · DOI: 10.3390/ma19030539 · Materials · 2026-01-29

## TL;DR

This review explores how polymeric fibers can be designed to either promote or prevent blood clotting by understanding their interactions with blood components.

## Contribution

The paper provides a unified framework linking molecular coagulation mechanisms with design strategies for procoagulant and anticoagulant polymeric fibers.

## Key findings

- Natural and synthetic polymers influence coagulation through interactions with plasma proteins and platelets.
- Surface chemistry and fiber morphology significantly modulate thrombogenicity and hemostasis.
- Emerging strategies include metal-polymer coordination and nanoscale texturing to control coagulation responses.

## Abstract

Fiber-forming polymers are increasingly used to control blood coagulation, either by accelerating the onset of hemostasis or by limiting thrombogenic events in contact with blood. Despite rapid progress in materials engineering, a unified view linking the molecular mechanisms of the coagulation cascade with specific design strategies of procoagulant and anticoagulant polymeric fibers is still missing. In this review, we summarize current knowledge on how natural and synthetic polymers interact with plasma proteins, platelets, and coagulation factors, emphasizing the role of fiber morphology, surface chemistry, charge distribution, and functionalization. Particular attention was paid to systems based on natural polysaccharides (e.g., chitosan, alginate, and cellulose derivatives), as well as synthetic polymers (e.g., PLA, PCL, polyurethanes, and zwitterionic materials). Two possible courses of action were described: their bioactivity may activate the contact pathway and/or support platelet adhesion or their ability to minimize protein adsorption and inhibit thrombin generation. We discuss how metal–polymer coordination, surface immobilization of heparin or nitric oxide donors, and nanoscale texturing modulate coagulation kinetics in opposite directions. Finally, we highlight emerging fiber-based strategies for achieving either rapid hemostasis or long-term hemocompatibility and propose design principles enabling precise tuning of coagulation responses for wound dressings, vascular grafts, and blood-contacting devices. This general compendium of knowledge on blood–material interactions provides a foundation for further design of biomaterials based on fiber-forming polymers and the development of manufacturing processes.

## Linked entities

- **Proteins:** F2 (coagulation factor II, thrombin)
- **Chemicals:** chitosan (PubChem CID 129662530), alginate (PubChem CID 5102882), PLA (PubChem CID 1018), nitric oxide (PubChem CID 145068)

## Full-text entities

- **Genes:** F2 (coagulation factor II, thrombin) [NCBI Gene 2147] {aka PT, RPRGL2, THPH1}
- **Diseases:** blood coagulation (MESH:D001778)
- **Chemicals:** PLA (MESH:C033616), nitric oxide (MESH:D009569), metal (MESH:D008670), cellulose (MESH:D002482), heparin (MESH:D006493), chitosan (MESH:D048271), polyurethanes (MESH:D011140), polysaccharides (MESH:D011134), alginate (MESH:D000464), polymer (MESH:D011108)

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12898453/full.md

## References

115 references — full list in the complete paper: https://tomesphere.com/paper/PMC12898453/full.md

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Source: https://tomesphere.com/paper/PMC12898453