Jason Mazow
The fibro proliferative disease Keloid Disorder (KD) is characterized by excessive dermal collagen deposition in response to skin injury and/or inflammation. Treatment for KD remains empirical and unsatisfactory despite much study. Through its direct influence and the resulting hypertension, activation of the Renin-Angiotensin System (RAS) causes fibrosis in many organs as well as immune system activation. The greater frequency of KD among dark-skinned people who are prone to vitamin D deficiency (VDD) and hypertension, as well as the link between KD and hypertension and VDD, both of which are linked to increased RAS activity, shed light on the etiology of KD. Embryonic-like Stem (ESC) cells that exhibit ESC markers inside Keloid-Associated Lymphoid Tissues (KALTs) are increasingly being linked to keloid lesions. The RAS, catharsis B, D, and G, which form RAS bypass loops, and the Vitamin D Receptor (VDR) are all expressed in these primitive cells. This shows that the RAS, both directly and through signalling pathways that converge on it, such as VDR-mediated processes and the immune system, may be important in controlling the primitive population within the KALTs. The importance of the RAS in controlling the ESC-like cells inside the KALTs, as well as its interaction with hypertension, vitamin D, VDR, VDD, and the immune system. By manipulating the RAS and its bypass loops and convergent signalling pathways, these ESC-like cells may be a unique therapeutic target for the treatment of this puzzling and demanding disorder.