Clot Retraction: Cellular Mechanisms and Inhibitors, Measuring Methods, and Clinical Implications

Abstract

Platelets have important functions in hemostasis. Best investigated is the aggregation of platelets for primary hemostasis and their role as the surface for coagulation leading to fibrin- and clot-formation. Importantly, the function of platelets does not end with clot formation. Instead, platelets are responsible for clot retraction through the concerted action of the activated αIIbβ3 receptors on the surface of filopodia and the platelet’s contractile apparatus binding and pulling at the fibrin strands. Meanwhile, the signal transduction events leading to clot retraction have been investigated thoroughly, and several targets to inhibit clot retraction have been demonstrated. Clot retraction is a physiologically important mechanism allowing: (1) the close contact of platelets in primary hemostasis, easing platelet aggregation and intercellular communication, (2) the reduction of wound size, (3) the compaction of red blood cells to a polyhedrocyte infection-barrier, and (4) reperfusion in case of thrombosis. Several methods have been developed to measure clot retraction that have been based on either the measurement of clot volume or platelet forces. Concerning the importance of clot retraction in inborn diseases, the failure of clot retraction in Glanzmann thrombasthenia is characterized by a bleeding phenotype. Concerning acquired diseases, altered clot retraction has been demonstrated in patients with coronary heart disease, stroke, bronchial asthma, uremia, lupus erythematodes, and other diseases. However, more studies on the diagnostic and prognostic value of clot retraction with methods that have to be standardized are necessary.

SARS-CoV-2 Spike Protein and Neutralizing Anti-Spike Protein Antibodies Modulate Blood Platelet Function

“…Thus, a clot becomes smaller, and excess fluid is extruded. Clot retraction is a physiologically important mechanism allowing the close contact of platelets in primary hemostasis, the reduction in wound size, and reperfusion in case of thrombosis [ 38 ]. However, the greater platelet number and fibrin crosslinking have the overall effect of increasing fibrin density and reducing clot permeability and pore size, which affects fibrinolysis.…”

Parallel repair mechanisms in plants and animals

“…When a vertebrate animal is wounded, platelets or their equivalents leak from ruptured blood vessels adjacent to the wound site, become activated and degranulate upon exposure to extravascular factors, including collagen ( Ivanciu and Stalker, 2015 ). Simultaneously, thrombin cleaves fibrin to fibrinogen to form a cross-linked mesh at the wound site, and the platelets become embedded in this mesh, forming a clot ( Martin, 1997 ; Jansen and Hartmann, 2021 ; Li et al, 2010 ). In insects, a similar localised release of vesicular granules and formation of a coagulatory fibrillar network occurs, although there are no platelet equivalents and few, if any, molecular parallels to vertebrate clotting ( Schmid et al, 2019 ).…”

Optimizing Extractability, Phytochemistry, Acute Toxicity, and Hemostatic Action of Corn Silk Liquid Extract

“…e degree of peeling of the blood clot and the volume of serum was assessed a day later. e retraction index was determined by dividing the volume of serum separated by the total volume of blood drawn for the trial (3 ml) [36].…”