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What Is The Main Function Of Blood Platelets

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Platelet Heterogeneity In Myeloproliferative Neoplasms

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Department of Physiology, Center for Advanced Medical and Pharmaceutical Research, “George Emil Palade” University of Medicine, Pharmacy, Science and Technology of Târgu Mureș, 540142 Târgu Mureș, Romania

Received: October 1, 2022 / Revised: October 20, 2022 / Accepted: October 21, 2022 / Published: October 23, 2022

Solved Describe The Function Of Platelets. Multiple Choice

Hemostasis is a physiological process critical for survival. However, thrombosis is among the leading causes of death worldwide, making antithrombotic therapy one of the most crucial aspects of modern medicine. Although antithrombotic therapy has progressed tremendously over the years, it remains far from ideal, and this is primarily due to incomplete understanding of the exceptionally complex structural and functional properties of platelets. However, advances in biochemistry, molecular biology and the advent of “omics” continue to provide crucial information for our understanding of the complex structure and function of platelets, their interactions with the coagulation system and their role in hemostasis and in thrombosis. In this review, we provide a comprehensive overview of the complex role that platelets play in hemostasis and thrombosis, and discuss the main clinical implications of these fundamental blood components, with a focus on platelet-related hemostatic disorders and existing and emerging antithrombotic therapies. We also emphasize a number of questions that still need to be answered and identify critical points for future research.

Since their initial description in the 1870s, it had become clear that platelets were exceptional cells that would never cease to amaze the scientific community. It soon became clear that although platelets circulate singly in the blood, they can rapidly form aggregates at sites of vascular injury [1], contributing to both hemostasis and thrombotic disease. However, at that time, the platelet saga was only in its infancy. Observations spanning more than half a century demonstrate that, in addition to their classic role in clot formation, platelets perform extremely versatile functions in many areas of physiology. Platelet α granules express receptors that facilitate adhesion to other vascular cells and release a wide variety of mediators that participate in and regulate functions such as chemotaxis, stem cell localization, cell migration, proliferation and differentiation, inflammation, angio- and lymphangiogenesis, the maintenance of lymphatic and blood systems as separate entities, deposition of matrix proteins, host defense, viral replication, information transport, vasomotor function and many others. Through this multitude of functions, platelet α-granules contribute to a wide range of physiological and pathological processes [2]. Activated platelets release a wide range of growth and angiogenic factors, cytokines and chemokines (Table 1). Once released, these molecules act to regulate chemotaxis, inflammation and vasomotor function, essential for restoring the integrity of injured vascular walls, for angiogenesis and for the growth of new blood vessels in areas of injured tissue. These characteristics provide platelets with tremendous potential for wound healing and tissue regeneration, as already demonstrated in settings such as diabetic ulcers, bone or tendon defects, maxillofacial and dental surgery, and corneal diseases [3]. It has also been suggested that platelets could promote rejuvenation and reverse aging by acting as a “fountain of youth” [4], although many of these applications are not yet supported by adequate evidence from clinical trials.

However, in parallel, activated platelets also cause changes in white blood cells and endothelial cells and release inflammatory mediators, thus promoting atherosclerosis and atherothrombosis, intimal vascular proliferation and post-angioplasty restenosis, and tumor growth, metastasis and immune evasion, in addition to amplifying inflammatory states. and infectious [2]. Studies have also shown that platelets release bioactive antimicrobial peptides and kinocidins and exhibit antimicrobial host defense properties, possessing unequivocal structural and functional characteristics of immune system cells [5]. Platelets thus play central roles as part of the intravascular innate immune system and coordinate the host’s adaptive antimicrobial defense, thus bridging innate and adaptive anti-infective immunity. There is evidence that platelets play complex roles in malaria, dengue, sepsis, and rheumatic disease infections, and deficiencies in platelet quantity or quality are increasingly recognized as correlates of infection risk and severity [6]. Furthermore, it has been demonstrated that there are complex interactions between the inflammatory and hemostatic functions of platelets. A prothrombotic platelet phenotype (involving platelet activation and platelet consumption leading to thrombocytopenia) can be observed in conditions with genetic deficiency in complement regulation, such as atypical hemolytic uremic syndrome or paroxysmal nocturnal hemoglobinuria [7].

Platelets, therefore, have a multitude of multifaceted functions. However, the main role of platelets continues to be the maintenance of normal hemostasis, in conjunction with the coagulation system. The classical theory of hemostasis (Figure 1A) describes a three-step process during which: (1) immediately after vascular injury, the injured vessel undergoes vasoconstriction to limit blood loss at the site of injury; (2) platelets adhere to the wall of the injured vessel, activate and form aggregates, that is, the platelet plug; which (3) is eventually stabilized by a dense fibrin meshwork formed through the coagulation cascade. In reality, however, this process is much more complex. The three phases that guarantee hemostasis are by no means independent and their activation is not precisely sequential. Instead, the three main processes that imply normal hemostasis activate simultaneously and continuously enhance each other throughout the hemostatic process (Figure 1B). In particular, the contribution of platelets to hemostasis far exceeds their simple participation in “primary hemostasis”, and the multiple interactions that exist between platelets, the vessel wall and the coagulation system complicate the fundamental process of hemostasis.

Blood: Function, What It Is & Why We Need It

In this review, we aim to provide a comprehensive overview of the complex role that platelets play in hemostasis and thrombosis, and discuss the main clinical implications of these fundamental blood components, with a focus on platelet-related hemostatic disorders and existing and emerging antithrombotics. therapies. We also emphasize a number of questions that still need to be answered and identify critical points for future research.

Platelets are small (≈2–4 μm), short-lived (≈8–10 days) anucleated cell fragments derived from the megakaryocyte lineage. Most platelets circulate in the bloodstream singly in a resting discoid form, without interacting with the vessel wall but continually monitoring the surrounding environment through a wide range of receptors and adhesion molecules and are finally eliminated from the blood at the end of its useful life. . Therefore, continuous platelet production is necessary to maintain normal platelet counts (i.e., 150–400 × 10

In response to vascular injury, platelets activate and quickly reveal their highly dynamic nature: they undergo enormous changes in shape and ultrastructure, including the “wrinkling” of their plasma membranes due to the emergence of cytoplasmic projections, causing them to assume a “ameboid form”. . At the same time, platelets undergo centralization and granule discharge. These critical ultrastructural changes mediated by the platelet cytoskeleton allow platelets to adhere to the site of vascular damage, spread throughout the injured area, release the contents of intracytoplasmic granules, and aggregate with other activated platelets to form the platelet plug, while simultaneously promoting fibrin. formation and repair of the vessel wall. Critical constituents for hemostasis are located both on the surface of the platelet membrane and in the cytoplasm, mainly within the granules (Figure 2).

The outer surface of resting circulating platelets is covered by a layer of glycolipid and glycoprotein molecules that form a prominent glycocalyx. With its net negative electrical charge, the glycocalyx provides a repulsive surface that prevents spontaneous platelet aggregation with other platelets or other blood or endothelial cells [8], while also playing a role in regulating calcium signaling [9] and platelet renewal [10].

Platelet Proteomes, Pathways, And Phenotypes As Informants Of Vascular Wellness And Disease

A wide variety of

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