Beta‐catenin non‐canonical pathway: A potential target for inflammatory and hyperproliferative state via expression of transglutaminase 2 in psoriatic skin keratinocyte

Abstract

Psoriasis is a chronic, local as well as a systemic, inflammatory skin condition. Psoriasis influences the quality of life up to 3.8% of the population and occurs often between 15 and 30 years of age. Specific causes are linked to psoriasis, including the interleukin IL-23/IL-17 Axis, human antigen leucocyte (HLA), and tumor necrosis factor-α (TNF-α). Secukinumab is a monoclonal antibody that specifically binds and neutralizes IL-17A required in the treatment of Psoriasis. The signaling pathways of Wnt govern multiple functions of cell-like fate specification, proliferation, polarity, migration, differentiation with their signaling controlled rigorously, given that dysregulation caused by various stimuli, can lead to alterations in cell proliferation, apoptosis, and human inflammatory disease. Current data has supported non-canonical Wnt signaling pathways in psoriasis development, particularly Wnt5a activated signaling cascades. These interconnected factors are significant in interactions between immune cells, keratinocytes, and inflammatory factors due to a higher degree of transglutaminase 2, mediated by activation of the keratinocyte hyperproliferation of the psoriatic patient's epidermis. This study discusses the pathology of Wnt5a signaling and its involvement in the epidermal inflammatory effects of psoriasis with other related pathways.

Role of platelet rich plasma mediated repair and regeneration of cell in early stage of cardiac injury

“…Reperfusion is now a routine therapy for MI, although it might lead to a malfunctioning in cardiomyocytes known as ischemic reperfusion injury (IRI) [ 29 ]. Although great progress has been made in identifying prospective pharmacological targets, no particular therapy is yet available for myocardial injuries in MI patients [ 30 , 31 ]. Appropriate atherosclerotic coronary artery pharmacomechanical revascularization reduces acute MI mortality.…”

The hair follicle‐psoriasis axis: Shared regulatory mechanisms and therapeutic targets

“…111,112 Moreover, imiquimod induces anagen in telogen HFs, along with perifollicular macrophage infiltrates. 113 Since none of the above mediators whose secretion is stimulated by imiquimod is a known anagen inducer, Wnt-releasing skin macrophage populations that promote both, anagen development 70,114 and psoriatic lesions, 77,115,116 might be one missing link in the HF-psoriasis axis. Yet, their role in imiquimod-induced psoriatic lesions and anagen induction remains to be investigated.…”

A molecular explanation of cardiovascular protection through abnormal cannabidiol: Involving the dysfunctional β‐adrenergic and ATP‐sensitive K+ channel activity in cardiovascular compromised preterm infants

“…Alternatively, the spike in β-AR numbers may be a stress reaction to heart injury. [83][84][85] Importantly, another study reported that animals exposed to adrenergic agonists fully depleted the rise in HI-induced β-AR numbers and often lowered AR messenger RNA to values smaller than those in HI-exposed animals alone. [4] The β-ARs expression in the premature heart is smaller than that at birth, which could clarify the impaired cardiovascular function in premature infants and their persistent failure of treatment with adrenergic agonists.…”