Nuclear factor erythroid 2-related factor 2 (Nrf2), a transcriptional factor that maintains intracellular redox equilibrium, modulates the expression of antioxidant genes, scavenger receptors, and cholesterol efflux transporters, all of which contribute significantly to foam cell development and plaque formation. Nrf2 has recently emerged as a key regulator that connects autophagy and vascular senescence in atherosclerosis. Autophagy, a cellular mechanism involved in the breakdown and recycling of damaged proteins and organelles, and cellular senescence, a state of irreversible growth arrest, are both processes implicated in the pathogenesis of atherosclerosis. The intricate interplay of these processes has received increasing attention, shedding light on their cumulative role in driving the development of atherosclerosis. Recent studies have revealed that Nrf2 plays a critical role in mediating autophagy and senescence in atherosclerosis progression. Nrf2 activation promotes autophagy, which increases lipid clearance and prevents the development of foam cells. Meanwhile, the activation of Nrf2 also inhibits cellular senescence by regulating the expression of senescence markers to preserve cellular homeostasis and function and delay the progression of atherosclerosis. This review provides an overview of the molecular mechanisms through which Nrf2 connects cellular autophagy and vascular senescence in atherosclerosis. Understanding these mechanisms can provide insights into potential therapeutic strategies targeting Nrf2 to modulate cellular autophagy and vascular senescence, thereby preventing the progression of atherosclerosis.

Nuclear factor erythroid 2-related factor 2 (Nrf2), a transcriptional factor that maintains intracellular redox equilibrium, modulates the expression of antioxidant genes, scavenger receptors, and cholesterol efflux transporters, all of which contribute significantly to foam cell development and plaque formation. Nrf2 has recently emerged as a key regulator that connects autophagy and vascular senescence in atherosclerosis. Autophagy, a cellular mechanism involved in the breakdown and recycling of damaged proteins and organelles, and cellular senescence, a state of irreversible growth arrest, are both processes implicated in the pathogenesis of atherosclerosis. The intricate interplay of these processes has received increasing attention, shedding light on their cumulative role in driving the development of atherosclerosis. Recent studies have revealed that Nrf2 plays a critical role in mediating autophagy and senescence in atherosclerosis progression. Nrf2 activation promotes autophagy, which increases lipid clearance and prevents the development of foam cells. Meanwhile, the activation of Nrf2 also inhibits cellular senescence by regulating the expression of senescence markers to preserve cellular homeostasis and function and delay the progression of atherosclerosis. This review provides an overview of the molecular mechanisms through which Nrf2 connects cellular autophagy and vascular senescence in atherosclerosis. Understanding these mechanisms can provide insights into potential therapeutic strategies targeting Nrf2 to modulate cellular autophagy and vascular senescence, thereby preventing the progression of atherosclerosis.

Nuclear factor erythroid 2-related factor 2 (Nrf2), a transcriptional factor that maintains intracellular redox equilibrium, modulates the expression of antioxidant genes, scavenger receptors, and cholesterol efflux transporters, all of which contribute significantly to foam cell development and plaque formation. Nrf2 has recently emerged as a key regulator that connects autophagy and vascular senescence in atherosclerosis. Autophagy, a cellular mechanism involved in the breakdown and recycling of damaged proteins and organelles, and cellular senescence, a state of irreversible growth arrest, are both processes implicated in the pathogenesis of atherosclerosis. The intricate interplay of these processes has received increasing attention, shedding light on their cumulative role in driving the development of atherosclerosis. Recent studies have revealed that Nrf2 plays a critical role in mediating autophagy and senescence in atherosclerosis progression. Nrf2 activation promotes autophagy, which increases lipid clearance and prevents the development of foam cells. Meanwhile, the activation of Nrf2 also inhibits cellular senescence by regulating the expression of senescence markers to preserve cellular homeostasis and function and delay the progression of atherosclerosis. This review provides an overview of the molecular mechanisms through which Nrf2 connects cellular autophagy and vascular senescence in atherosclerosis. Understanding these mechanisms can provide insights into potential therapeutic strategies targeting Nrf2 to modulate cellular autophagy and vascular senescence, thereby preventing the progression of atherosclerosis.

Nuclear factor erythroid 2-related factor 2 (Nrf2), a transcriptional factor that maintains intracellular redox equilibrium, modulates the expression of antioxidant genes, scavenger receptors, and cholesterol efflux transporters, all of which contribute significantly to foam cell development and plaque formation. Nrf2 has recently emerged as a key regulator that connects autophagy and vascular senescence in atherosclerosis. Autophagy, a cellular mechanism involved in the breakdown and recycling of damaged proteins and organelles, and cellular senescence, a state of irreversible growth arrest, are both processes implicated in the pathogenesis of atherosclerosis. The intricate interplay of these processes has received increasing attention, shedding light on their cumulative role in driving the development of atherosclerosis. Recent studies have revealed that Nrf2 plays a critical role in mediating autophagy and senescence in atherosclerosis progression. Nrf2 activation promotes autophagy, which increases lipid clearance and prevents the development of foam cells. Meanwhile, the activation of Nrf2 also inhibits cellular senescence by regulating the expression of senescence markers to preserve cellular homeostasis and function and delay the progression of atherosclerosis. This review provides an overview of the molecular mechanisms through which Nrf2 connects cellular autophagy and vascular senescence in atherosclerosis. Understanding these mechanisms can provide insights into potential therapeutic strategies targeting Nrf2 to modulate cellular autophagy and vascular senescence, thereby preventing the progression of atherosclerosis.

The new coronavirus disease (COVID-19) outbreak has challenged us to take unprecedented steps to bring this pandemic under control. In view of the urgency of this situation, convalescent plasma which was used in previous coronavirus outbreaks has emerged as one of the treatment options in this current pandemic. This is mainly due to the fact that convalescent plasma has been studied in a few case series with promising outcomes. In addition, on-going large clinical trials aimed to further evaluate the effectiveness, safety, and optimal dosage, duration and timing of administration of convalescent plasma are indeed revealing a certain level of promising results. Therefore, this article aims to provide an overview of possible mechanisms of actions of convalescent plasma, its benefits and its level of usage safeness by summarizing the existing evidence on the use of convalescent plasma in COVID-19 patients.