Department of Health Sciences and Sport Medicine, Hungarian University of Sports Sciences, 1123 Budapest, Hungary.
Int J Mol Sci. 2022 Oct 8;23(19):11940. doi: 10.3390/ijms231911940.
Psoriasis is considered a multifactorial and heterogeneous systemic disease with many underlying pathologic mechanisms having been elucidated; however, the pathomechanism is far from entirely known. This opinion article will demonstrate the potential relevance of the somatosensory Piezo2 microinjury-induced quad-phasic non-contact injury model in psoriasis through a multidisciplinary approach. The primary injury is suggested to be on the Piezo2-containing somatosensory afferent terminals in the Merkel cell−neurite complex, with the concomitant impairment of glutamate vesicular release machinery in Merkel cells. Part of the theory is that the Merkel cell−neurite complex contributes to proprioception; hence, to the stretch of the skin. Piezo2 channelopathy could result in the imbalanced control of Piezo1 on keratinocytes in a clustered manner, leading to dysregulated keratinocyte proliferation and differentiation. Furthermore, the author proposes the role of mtHsp70 leakage from damaged mitochondria through somatosensory terminals in the initiation of autoimmune and autoinflammatory processes in psoriasis. The secondary phase is harsher epidermal tissue damage due to the primary impaired proprioception. The third injury phase refers to re-injury and sensitization with the derailment of healing to a state when part of the wound healing is permanently kept alive due to genetical predisposition and environmental risk factors. Finally, the quadric damage phase is associated with the aging process and associated inflammaging. In summary, this opinion piece postulates that the primary microinjury of our “sixth sense”, or the Piezo2 channelopathy of the somatosensory terminals contributing to proprioception, could be the principal gateway to pathology due to the encroachment of our preprogrammed genetic encoding.
银屑病被认为是一种多因素和异质性的系统性疾病,其许多潜在的病理机制已经阐明;然而,发病机制远未完全清楚。本文将通过多学科的方法,展示感觉 Piezo2 微损伤诱导的四相非接触性损伤模型在银屑病中的潜在相关性。初步损伤被认为发生在含有 Piezo2 的感觉传入末梢的 Merkel 细胞-神经纤维复合体中,同时伴随着 Merkel 细胞中谷氨酸囊泡释放机制的损伤。部分理论认为,Merkel 细胞-神经纤维复合体有助于本体感觉;因此,对皮肤的拉伸。Piezo2 通道病可能导致 Piezo1 以簇状方式对角质形成细胞的不平衡控制,导致角质形成细胞增殖和分化失调。此外,作者提出了受损线粒体通过感觉末梢漏出线粒体 mtHsp70 在银屑病自身免疫和自身炎症过程中的起始作用。第二阶段是由于初步本体感觉受损导致的更严重的表皮组织损伤。第三损伤阶段是再损伤和致敏,由于遗传倾向和环境危险因素,愈合被脱轨,部分伤口愈合永久存活。最后,四相损伤阶段与衰老过程和相关的炎症老化有关。总之,这篇观点文章假设,我们“第六感”的初级微损伤,或参与本体感觉的感觉末梢的 Piezo2 通道病,可能是由于我们预先编程的遗传编码的侵犯,导致病理学的主要途径。