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Endothelial cell dysfunction and pre-eclampsia
Published in Pankaj Desai, Pre-eclampsia, 2020
Many markers have been identified in experimental and clinical investigations, which are supposed to indicate the endothelial activation process. They have been reported in pre-eclampsia and include: Increased circulating concentration of endothelin-1.5Increased levels of fibronectin in circulation.6Decreased levels of circulating vasodilator PGI2.7Altered levels of circulating thrombomodulin.8
Endothelial Cells
Published in John H. Barker, Gary L. Anderson, Michael D. Menger, Clinically Applied Microcirculation Research, 2019
Thus, despite their deceptive thinness in transverse section, ECs are highly active and responsive cells. It is clear from the foregoing discussion that ECs perform a multitude of functions, some constitutively and some that are induced following activation. It is not yet known whether all aspects of endothelial activation occur concomitantly; nevertheless, they share some common mechanisms of cellular signal transduction.
Pathogenesis
Published in Aparna Palit, Arun C. Inamadar, Systemic Sclerosis, 2019
The persistent endothelial activation results in endothelial damage leading to apoptosis. The inability to replace apoptotic cells leads to characteristic capillary breakdown.9 The endothelial activation leads to damage and apoptosis. These changes are detected during the early inflammatory stage, both in lSSc and dSSc. The activation of vascular endothelial cells with the release of the vasoactive mediators result in increased microvascular permeability corresponding to the early edematous phase in cutaneous manifestation of SSc. The activated endothelial cells show upregulation of vascular cell adhesion molecule-1(VCAM-1), ELAM-1, ET-1, intercellular adhesion molecule-1 (ICAM-1), and thrombomodulin. The latter three molecules are also upregulated during the apoptosis of endothelial cells. In SSc, the replacement of apoptotic endothelial cells is impaired and results in capillary breakdown. The endothelial injury not only causes vasculopathy, but also exposes sub-endothelial layers to the immune system.2 The endothelial injury can also occur due to antibody-dependent cell-mediated cytotoxicity mediated by IgG antibodies and proteolytic activities present in serum.1
Morphological changes without histological myocarditis in hearts of COVID-19 deceased patients
Published in Scandinavian Cardiovascular Journal, 2022
Ali Razaghi, Attila Szakos, Riham Al-Shakarji, Mikael Björnstedt, Laszlo Szekely
Endothelial activation was detected in all cases independently if local prolonged ischemia (shown as WT-1 induction) was evident. A possible explanation for this phenomenon is that the endothelium activating agent was not originating from the local hypoxic tissue but from other sites in the body, e.g. from the consolidated hypoxic areas of the Covid-19 lungs. The most likely explanation for the endothelial activation is the presence of circulating VEGF that is known to be produced in the Covid-19 lungs in large quantities [27]. In addition, immunohistochemical staining (CD31 and CD146) showed signs of endothelial activation due to the enlarged fibroblast-like endothelial cells with activated euchromatic nuclei. Our study showed the activation of the endothelium in the form of aggregation of fibroblastoid cells with vacuolated cytoplasm leading to further capillary formation [29].
Endothelial dysfunction sustains immune response in atherosclerosis: potential cause for ineffectiveness of prevailing drugs
Published in International Reviews of Immunology, 2022
Endothelial activation and dysfunction precede the development of atherosclerotic lesion formation. A plethora of factors can actuate endothelial activation, and persistence of these factors leads to its dysfunction. For the development of atherosclerotic lesions, endothelial dysfunction (ED) in conjunction with immune activation is essential. Factors triggering ED are also known to elicit immune cell activation. For example, hypercholesterolemia besides prompting ED also causes neutrophilia, platelet–leukocyte aggregates, monocytosis, monocyte activation, T-cell receptor (TCR) stimulation, T-cell proliferation and differentiation to T helper (Th)2, Th17 phenotype and regulatory T (Treg) cell development in experimental models and patients [1–8]. On the same note, hyperhomocystenemia besides inducing ED also stimulates chemokine/cytokine production in monocytes as well as T cells and leads to the formation of active neutrophil extracellular traps (NETosis) and platelet aggregation [9–14]. Hypertension causes expression of the damage-activated molecular pattern (DAMP) and neoantigens, which in turn activates antigen-presenting cells such as dendritic cells (DCs) to a proinflammatory phenotype. These activated DCs then drift to secondary lymphoid organs where they initiate maturation of inflammatory T effector lymphocytes such as Th1 or Th17 leading to a vascular inflammatory response [15]. Once ED is established it sustains immune cell activation by continually expressing and/or secreting different molecules, and particles contributing to atherosclerotic lesion growth.
Endothelial dysfunction and vascular complications after allogeneic hematopoietic cell transplantation: an expert analysis
Published in Expert Review of Hematology, 2021
Ioannis Eftychidis, Ioanna Sakellari, Achilles Anagnostopoulos, Eleni Gavriilaki
A renal biopsy would confirm the diagnosis of TA-TMA, although it is not a common practice because of the vulnerability of the HCT recipients [59,60]. Therefore, its diagnosis is based on routine laboratory markers, with the International Working Group Criteria evaluating the presence of: schistocytes >4%, elevated lactate dehydrogenase (LDH), thrombocytopenia, anemia, decreased haptoglobin. Addition of complement markers as prognostic or diagnostic factors of TA-TMA has revolutionized the field [52]. Indeed, functional and genetic evidence have proven the involvement of complement activation as a key factor of TA-TMA pathophysiology in both the pediatric and adult population [35,61,62]. Given the lack of wide accessibility of these markers, prediction of endothelial damage has also been explored by calculating the endothelial activation and stress index (‘EASIX’) using routine laboratory biomarkers. EASIX has been associated with complement activation in TA-TMA, predicting survival in these patients [63]. A larger study has also shown that EASIX predicted TA-TMA and poor survival post alloHCT [64].