Is the new angel better than the old devil? Challenges and opportunities in CD47- SIRPα-based cancer therapy.

The efficacy of immunotherapies is limited due to the impenetrable nature of the tumor microenvironment (TME). The TME of many tumors is immune-privileged, thus allowing them to evade host immunosurveillance. One mechanism through which this occurs is via the overexpression of CD47, a 'don't eat me' protein that can interact with SIRPα on myeloid cells to suppress their phagocytic action.

Direct Keap1-kelch inhibitors as potential drug candidates for oxidative stress-orchestrated diseases: A review on In silico perspective.

The recent outcry in the search for direct keap1 inhibitors requires a quicker and more effective drug discovery process which is an inherent property of the Computer Aided Drug Discovery (CADD) to bring drug candidates into the clinic for patient's use. This Keap1 (negative regulator of ARE master activator) is emerging as a therapeutic strategy to combat oxidative stress-orchestrated diseases. The advances in computer algorithm and compound databases require that we highlight the functionalities that this technology possesses that can be exploited to target Keap1-Nrf2 PPI.

Neurotrophic, anti-neuroinflammatory, and redox balance mechanisms of chalcones.

The passage of time that evoke aging; the tilted redox balance that contribute oxidative entropy; the polarization of microglia cells that produce inflammatory phenotype; all represent the intricacies of CNS-dependent disease progression. Neurological diseases that result from CNS injury raise social concerns and the available therapeutic strategies are frustrated by low efficacy, high toxicity, and multiple side effects. However, emergent studies have shown the neuroprotective role of natural compounds - including chalcones - with high efficacy in the protection of CNS structures.

AMPK allostery: A therapeutic target for the management/treatment of diabetic nephropathy.

Diabetic nephropathy (DN) is a chronic complication of diabetes mellitus (DM) with approximately 30-40% of patients with DM developing nephropathy, and it is the leading cause of end-stage renal diseases and diabetic morbidity. The pathogenesis of DN is primarily associated with irregularities in the metabolism of glucose and lipid leading to hyperglycemia-induced oxidative stress, which has been a major target together with blood pressure regulation in the control of DN progression. However, the regulation of 5' adenosine monophosphate-activated protein kinase (AMPK), a highly conserved protein kinase for maintaining energy balance and cellular growth and repair has been implicated in the development of DM and its complications.