Regeneration of the vascular compartment

Abstract

Throughout life, damage to the vascular endothelium is pivotal in the development of cardiovascular disease. Therefore, a detailed understanding of the underlying mechanisms involved in endothelial cell restoration is of fundamental importance for preventive and therapeutic concepts in cardiovascular disease. The goal of regenerative medicine is the use of tissue-specific progenitor cells for a more effective repair process with reduction of fibrocellular remodelling, fibrosis and loss of functional properties.According to the hitherto assumed primary model of endothelial regeneration only adjacent and intact mature endothelial cells replace damaged endothelium. Since Asahara and colleagues first described that a peripheral blood mononuclear cell population was able to differentiate into endothelial cells in vitro and incorporate into ischemic tissue at sites of angiogenesis in vivo, the model of endothelial regeneration has been extended. The majority of clinical trials on human cell therapy for ischemic vascular disease are based on cell surface antigen expression of CD34 or VEGFR2 to identify endothelial progenitor cells.A precise characterization of the angiogenic properties of different subsets of endothelial regenerating cells and their course of action to gain sufficient long-term regeneration of the injured vessel is a necessary precondition before clinical trials of human cell therapy become a routine reality.

Infections and cardiovascular disease: is Bartonella henselae contributing to this matter?

“…Interestingly, further studies associated the presence/absence of surface markers with specific functionalities of EPCs, like vascular homing and repair competence, incorporation into the damaged endothelium, and in vivo vessel formation (Asahara et al, 1997;Becher et al, 2010;Friedrich et al, 2006;Hur et al, 2004;Sieveking et al, 2008).…”

The role of stem cells in adipose tissue remodeling.

“…Moreover, we find that HFD appears to decrease the proliferation of tissue-resident cells, suggesting that, these resident EPCs might have decreased proliferative capacity and contribute to pathological adipose tissue remodeling. This is important because decreased levels of these pro-angiogenic cells have been implicated in the development of several chronic diseases including cardiovascular disease, due likely to a diminished capacity to repair damaged vasculature (73)(74)(75)(76)(77)(78). Obesity along with exposure to other environmental factors, i.e.…”

“…Levels of these cells can be influenced not only by obesity, but by several environmental factors such as exposure to air pollution and components of cigarette smoke (68,69,71,72 (68,69,71,(80)(81)(82). Taken together, it can be concluded that EPCs function to repair damaged vasculature in order to maintain adequate tissue oxygenation, preventing further ischemia-induced cell death and fibrosis (75). Interestingly, the term "EPC" is a general one describing a variety of cell types that have been shown to promote angiogenesis or vessel repair (68,69,71,75,80,82 …”

“…Taken together, it can be concluded that EPCs function to repair damaged vasculature in order to maintain adequate tissue oxygenation, preventing further ischemia-induced cell death and fibrosis (75). Interestingly, the term "EPC" is a general one describing a variety of cell types that have been shown to promote angiogenesis or vessel repair (68,69,71,75,80,82 …”

“…There is also evidence that these adipose tissue stem cells can impose paracrine effects, stimulating the migration of endothelial cells to prevent neointimal formation and promote vascular repair (37,52,66,169,182,183). Since stem cells play a role in several organ systems, the competency and levels of these cells could be crucial to their ability to provide adequate tissue support; however, both of these characteristics can be affected by several factors (52,68,69,73,75,82,168). In the obese condition, adipocytes can expand tremendously to accommodate the excess lipid load, and in some cases, adipocytes hypertrophy to 10,000 µm in diameter (184).…”