It is the cellular layer that covers the body’s blood vessels; it is highly resistant.
This tenuous structure constantly resists blood flow, hydrostatic pressure, stretching, and tissue compression to create a unique and highly dynamic barrier at a few hundred nanometers thick.
Which maintains a necessary structure that divides the tissues of the body’s circulatory system.
The endothelium is also highly adaptable.
In cases where the barrier must be physically violated to allow immune cells to reach various body regions to fight infections.
The endothelium cooperates with leukocytes to create openings that provide infection-fighting cells with immediate access to their targets.
These subsequent “micro-wounds” are ephemeral; as soon as the cells have crossed the endothelium, these pores and spaces heal quickly, restoring the efficient barrier function of the system.
When gaps do not close, and leaks occur, the results can lead to dramatic pathologies that include sepsis, acute lung injuries, ischemic cardiovascular diseases, and chronic inflammatory diseases such as diabetes and arthritis.
The endothelium forms the inner cell lining of all the blood and lymph vessels in the body and is an excellent example of where biology meets physics and engineering.
It must convert mechanical forces into chemical signals to maintain homeostasis.
The endothelium is located between the blood and the vascular wall and acts as a receptor and transmitter of signals.
These endothelial cells recognize hemodynamic changes in the blood and respond to these changes through numerous vasoactive, immune and metabolic processes by releasing numerous biologically active factors such as:
- Nitric oxide.
- Hyperpolarizing factor derived from the endothelium.
- Transforming growth factor.
- Vascular endothelial growth factor.
- The growth factor of primary fibroblasts.
- Growth factors are derived from platelets.
- Tissue plasminogen activator.
- Tissue plasminogen activator inhibitor type 1.
- Reactive oxygen species.
- Monocyte adhesion molecules.
These factors intervene in the tone and growth of the vascular smooth muscle and processes such as coagulation, fibrinolysis, and adhesion of blood cells to the vascular wall.
It also controls the immune response, drug administration through the vasculature, and cancer metastasis.
Endothelial dysfunction is a marker of preclinical atherosclerosis characterized by altered endothelium-dependent vasodilatation and a proinflammatory state that promotes the development of atherosclerosis.
Menopause marks an increase in endothelial dysfunction.
Compared with men, age-related endothelial dysfunction is attenuated in premenopausal, normotensive, and hypertensive women.
However, after menopause, there is a substantial decrease in endothelium-dependent vasodilation, and by age 60, there are no observable sex differences.
This indicates an association between endothelial dysfunction and reduction in endogenous estrogen production.
Markers of activation and endothelial dysfunction
Endothelial activation and dysfunction are characterized by a change in the balance of vasomotor factors released by the endothelium, inflammatory cytokines and chemokines, expression and secretion of selectins and adhesion molecules, and modulation of local thrombotic pathways.
It has been demonstrated that the measurement of the circulating levels of markers and relevant mediators of these pathways provide important physiopathological data on the influence of the endothelium in the processes of atherosclerotic diseases.
Although limited by the fact that the systemic levels of these biomarkers may not represent their local levels and activity in the vascular wall.
Endothelial cell injury typically accompanies vascular inflammation.
Therefore, fragments of activated endothelium, endothelial microparticles, and entire endothelial cells are poured into the circulation.
These can be measured in the blood, and their circulating levels increase in association with coronary endothelial dysfunction, unstable coronary syndromes, and vasculitis.
Role in endothelial hemostasis
The main reason why blood in the vascular system remains fluid is the presence of endothelium.
Endothelium actively participates in many physiological and pathological processes, is an active participant in hemostasis, works to decrease thrombosis, and, if damaged, promotes thrombosis through blood exposure to tissue factors.
This prostaglandin works to keep the vessels open (vasodilation).
It also prevents platelet aggregation by acting on platelets to increase cyclic adenosine monophosphate, effectively reducing the amount of thromboxane A2 that has procoagulant activities.
When platelets contact collagen, they produce adenosine diphosphate, further promoting platelet aggregation.
The endothelium produces nitric oxide in response to adenosine diphosphate of activated platelets.
This nitric oxide works to maintain vasodilatation, decreasing coagulation likelihood.
Protein C is released from the endothelium in response to thrombin and acts to inactivate some coagulation factors.
A substance similar to heparin is produced on the surface of endothelial cells that acts to inactivate thrombin.
The endothelial cells help dissolve the clot, releasing plasminogen activators; this is a key molecule involved in the breakdown of clots after they have formed.
Closing of the micro-wounds
The leukocytes generate ” invasive podosomes, “which produce vascular micro-wounds through an endothelial perforation.
When the endothelium detects an acute loss of isometric tension, in response, as a biomechanical signal, it generates reactive oxygen species, which are responsible for coordinating the process of closing the microbicide.