Cellular processes depend on Copper(Cu) homeostasis, but overload of Cu in cells leads to the disruption of that balance and induces a specialized model of regulated cell death known as cuproptosis. As opposed to the conventional cell death modalities, this mechanism features the connection of Cu ions with fatty-acylated elements of the TCA cycle, which subsequently promotes proteotoxic clustering and dysfunction of the mitochondria. Cuproptosis has a distinct and regulated pathway that is not responsive to standard cell demise inhibitors, which warrant its potential role in a number of pathophysiological mechanisms, specifically in the pathogenesis of inflammatory conditions and cancer. However, the disease-specific regulatory networks of its functioning cannot be comprehensively studied, and it has been a great challenge in regard to designing specific therapeutic developments. This paper critically analyzes the regulatory processes of copper equilibrium and cuproptosis, focusing on the important regulatory genes and their interaction networks. We describe pathological implications of cuproptosis in inflammation and malignancies, outline the recent intervention methods, and address the limitations of the current research such as lack of in vivo models and biomarkers. Not only do we offer a systematic source of information about biological importance of cuproptosis but also suggest novel knowledge about the specific treatment of inflammation and cancer which has a great theoretical value and promising opportunities of its practical implementation.
Liu et al. (Thu,) studied this question.