About this Research Topic
Ischemia-reperfusion injury (IRI) is a well-recognized pathological condition progressing from acute to chronic damage in various organs such as the heart, kidneys, liver, and brain. Particularly in the field of organ transplantation (including kidneys, hearts, lungs, livers, pancreas, and intestines), it is intensively studied as a factor contributing to organ dysfunction. Despite numerous studies on IRI across different organs, there remains a need for a better understanding of the related signaling pathways and identifying more effective therapeutic targets.
The goal of this Research Topic is to foster a comprehensive analysis of the transition from acute to chronic damage in IRI, and the associated acute organ damage. By collecting the latest research on molecular factors - including but not limited to ROS, ferroptosis, apoptosis, necrosis, inflammation, and fibrosis – we aim to shed light on critical signaling pathways and potentially therapeutic targets. We welcome a variety of studies ranging from research suggesting various mechanisms of damage to targets for prevention and treatment, including the effects of genetic alteration, temperature, and metabolic changes within cellular and animal models of IRI. The ultimate aspiration for this Research Topic is to inspire many studies aimed at recovering various organs from IR damage and effectively inhibiting organ dysfunction. In so doing, we hope to contribute significantly to the scientific community's understanding and approach towards IRI.
Areas to be covered may include but are not limited to:
• Novel suggestions in various damage mechanisms and their interconnected networks in ischemia-reperfusion, including oxidative stress, apoptosis, necrosis, ferroptosis, autophagy, ER stress, and inflammation.
• Novel suggestions for Prevention and Treatment, Including Preconditioning.
• Regenerative process after ischemia-reperfusion injury, including studies focused on the mechanism leading to fibrosis, and regeneration methods such as stem cells.
• Research about the effects of genetic abnormalities, temperature changes, and metabolic abnormalities on ischemia-reperfusion damage
A full list of accepted article types, including descriptions, can be found at this link.
The goal of this Research Topic is to foster a comprehensive analysis of the transition from acute to chronic damage in IRI, and the associated acute organ damage. By collecting the latest research on molecular factors - including but not limited to ROS, ferroptosis, apoptosis, necrosis, inflammation, and fibrosis – we aim to shed light on critical signaling pathways and potentially therapeutic targets. We welcome a variety of studies ranging from research suggesting various mechanisms of damage to targets for prevention and treatment, including the effects of genetic alteration, temperature, and metabolic changes within cellular and animal models of IRI. The ultimate aspiration for this Research Topic is to inspire many studies aimed at recovering various organs from IR damage and effectively inhibiting organ dysfunction. In so doing, we hope to contribute significantly to the scientific community's understanding and approach towards IRI.
Areas to be covered may include but are not limited to:
• Novel suggestions in various damage mechanisms and their interconnected networks in ischemia-reperfusion, including oxidative stress, apoptosis, necrosis, ferroptosis, autophagy, ER stress, and inflammation.
• Novel suggestions for Prevention and Treatment, Including Preconditioning.
• Regenerative process after ischemia-reperfusion injury, including studies focused on the mechanism leading to fibrosis, and regeneration methods such as stem cells.
• Research about the effects of genetic abnormalities, temperature changes, and metabolic abnormalities on ischemia-reperfusion damage
A full list of accepted article types, including descriptions, can be found at this link.
Keywords: apoptosis, necrosis, ferroptosis, autophagy, ER stress, inflammation, metabolic abnormality, oxidative stress, preconditioning, temperature
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
