The body’s innate mechanism for controlling bleeding is a process known as haemostasis. This is orchestrated through an intricate cascade of biochemical signals that ultimately weaves a mesh from a protein called fibrin. The mesh forms around red blood cells, generating a clot.
Natural blood clots have poor mechanical strength because of a profound structural imbalance: red blood cells can account for more than half of a clot’s volume, but contribute almost nothing to its mechanical integrity. Instead, they act as a passive cargo, trapped in a fibrin network that constitutes less than 1% of the clot’s total volume4. Consequently, natural clots are inherently vulnerable to rupture or dislodgement under physiological blood pressures, and frequently fail when subjected to a substantial mechanical stress.
Jiang et al. address the slow formation and poor strength of blood clots by introducing a technique that they call click clotting.
The first step is to chemically modify the surface of red blood cells by attaching molecules of an organic compound known as trans-cyclooctene. Next, the modified cells are mixed with a polymer to which chemical groups called tetrazines have been attached. The trans-cyclooctenes react rapidly with the tetrazines to form a cytogel — a continuous, load-bearing network of cells cross-linked by polymers.
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