**Figure 1.**

*OBESTITY and PROINFLAMATORY STATE.*

component of vessel wall remodeling in response to injury, which controls coagulation and fibrinolysis activities, reduces vascular tone and regulates cellular and vascular adhesions, inhibits leukocyte adhesions, and modulates inflammatory activities and angiogenesis (**Figure 2**).

**Vasodilators:** Apelin, H2S, NO, PGI2, IgF1. **Permeability:** NO, VEGF, ROS, PGI2, PAI1, FGF, Leptin. **Anticoagulant factors:** Anti thrombin III, Thrombomodulin. **Angiogenic factors:** FGF, TGFβ, VEGF. **Vasoconstrictors:** ROS, VCAM, PgH2, Ang II, Resistin. **Inflammatory mediators:** Leucotriens, integrins Inmunoglobulins. **Procoagulant factors:** TF, PAF, vWF, TXA2, PAI. **Proliferation:** NO, TxA2, ROS, PgH2.

*H2S: Hydrogen Sulfide, NO: Nitric Oxide,* PGI2*: Proctaciclin, IgF1: Insulin Like growth factor 1, VEGF: vascular endothelial growth factor, PAI1: Plaminogen Activator Inhibitor, FGF: Fibroblast Growth Factor, TGFβ: Transforming Growth Factor β, ROS: Reactive Oxygen Species, VCAM: Vascular Cell Adhesion Molecule1, PgH2: Prostaglandin H2, Ang II: Angiotensin II, TF: Tissue Factor; vWF: Von Willebrand Factor, PAF: Platelet Activating Factor, TXA2: thromboxane A2, PAI: Plasminogen Activator Inhibitor1.*

**Figure 2.** *Endothelial dysfunction and obesity.*

Nevertheless, the endothelial dysfunction is usually characterized by the disrupt between secretion and release of vasoconstriction and vasodilation agents, pushing the vascular endothelial toward prothrombotic and proatherogenic effects [23].

Secondly, the distorted provokes that the leukocyte adhesion, activation of platelets, pro-oxidation of mitogens, impaired PGI2, coagulation, and nitric oxide (NO) productions are the features or ¨faulty physiological properties¨ resulted from a dysfunction of endothelium, as well decreased synthesis of EDHF, and vasoconstriction factors including Ang II and prostaglandin (PGH2), atherosclerosis, and thrombosis (**Figure 3**) [23].

The major participating agents of endothelial dysfunction in obesity include: insulin resistance, oxidized form of low-density lipoprotein (oxLDL), adipose tissues related inflammation, and decreased NO bioavailability. Others such as elevated production of ROS and arginase, advanced glycation end products (RAGE), and phenotypic alterations in perivascular adipose tissue result in mild inflammation and elevated leptin with subsequent reduction of adiponectin secretions [24].

Further obesity generates a procoagulant state, which is explained by several mechanisms:


**Figure 3.**

*Proinflamatory and anti-inflammatory state in obesity.*

3.Inflammation has been characterized by the imbalance between proinflammatory and procoagulant, and anti-inflammatory and anticoagulant activities of the endothelium, leading to disturbance of the hemostatic system.
