Deeper insight into ferroptosis: association with Alzheimer's, Parkinson's disease, and brain tumors and their possible treatment by nanomaterials induced ferroptosis.

Ferroptosis is an emerging and novel type of iron-dependent programmed cell death which is mainly caused by the excessive deposition of free intracellular iron in the brain cells. This deposited free iron exerts a ferroptosis pathway, resulting in lipid peroxidation (LiPr). There are mainly three ferroptosis pathways viz. iron metabolism-mediated cysteine/glutamate, and LiPr-mediated. Iron is required by the brain as a redox metal for several physiological activities. Due to the iron homeostasis balance disruption, the brain gets adversely affected which further causes neurodegenerative diseases (NDDs) like Parkinson's and Alzheimer's disease, strokes, and brain tumors like glioblastoma (GBS), and glioma. Nanotechnology has played an important role in the prevention and treatment of these NDDs. A synergistic effect of nanomaterials and ferroptosis could prove to be an effective and efficient approach in the field of nanomedicine. In the current review, the authors have highlighted all the latest research in the field of ferroptosis, specifically emphasizing on the role of major molecular key players and various mechanisms involved in the ferroptosis pathway. Moreover, here the authors have also addressed the correlation of ferroptosis with the pathophysiology of NDDs and theragnostic effect of ferroptosis and nanomaterials for the prevention and treatment of NDDs.

Dysbiosis versus diabesity: Pathological signaling and promising therapeutic strategies.

A healthy life depends on the inseparable relationship between a host and the gut microbiota. A healthy gut microbiota regulates intestinal integrity, whereas an unbalanced gut microbiota contributes to junctional remodeling and leads to dysbiosis. Bacterial infiltration and dysbiosis are reported to activate a series of pathological cascades that trigger metabolic abnormalities, including diabesity. Conversely, recent studies revealed that the incidence of dysbiosis itself is fuelled by diabesity. In this review, we highlight the molecular aspects of multifaceted pathological signaling between dysbiosis and diabetes that could pave the way for new drug discovery. Moreover, to reinstate the gut microbiota and restrict the epidemic of dysbiosis and diabesity, we also scrutinize a promising therapeutic strategy that can challenge the pathological interlink.