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Updated: Jun 5, 2026

Ischemia-reperfusion Model of Acute Kidney Injury and Post Injury Fibrosis in Mice
Published on: August 9, 2013
Ischemic kidney injury and mechanisms of tissue repair
Marwa El Sabbahy1, Vishal S Vaidya
1Laboratory of Kidney Toxicology and Regeneration, Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Harvard Institutes of Medicine, Boston, MA, USA.
Abstract:
Acute kidney injury (AKI) may result from ischemia or by the use of nephrotoxic agents. The incidence of AKI is variable, depends on comorbidities, and ranges from 5 to 35% in all hospitalized patients. The mechanisms of kidney injury exist within a large network of signaling pathways driven by interplay of inflammatory cytokines/chemokines, reactive oxygen species (ROS), and apoptotic factors. The effects and progression of injury overlap extensively with the remarkable ability of the kidney to repair itself both by intrinsic and extrinsic mechanisms that involve specific cell receptors/ligands as well as possible paracrine influences. The fact that kidney injury is usually part of a generalized comorbid condition makes it all the more challenging in terms of assessment of severity. In this review, we attempt to analyze the mechanisms of ischemic injury and repair in acute and chronic kidney disease from the perspectives of both preclinical and human studies.
Insights
This review analyzes acute kidney injury (AKI) mechanisms, focusing on inflammation, oxidative stress, and apoptosis in both ischemic and nephrotoxic injury. It explores kidney repair processes and challenges in assessing severity due to comorbidities.
Area of Science:
- Nephrology
- Cellular Biology
- Pathophysiology
Background:
- Acute kidney injury (AKI) affects 5-35% of hospitalized patients, with incidence varying by comorbidities.
- Kidney injury involves complex signaling pathways including inflammatory cytokines, reactive oxygen species (ROS), and apoptotic factors.
- Assessing AKI severity is challenging due to its frequent association with generalized comorbid conditions.
Purpose of the Study:
- To analyze the mechanisms of ischemic injury in acute and chronic kidney disease.
- To review kidney repair mechanisms, including intrinsic and extrinsic factors.
- To integrate findings from preclinical and human studies on kidney injury and repair.
Main Methods:
- Literature review of preclinical and human studies.
- Analysis of signaling pathways involved in kidney injury.
- Examination of cellular repair mechanisms and paracrine influences.
Main Results:
- Kidney injury pathogenesis involves a complex interplay of inflammatory, oxidative, and apoptotic pathways.
- Kidney repair mechanisms are multifaceted, involving cell receptors, ligands, and paracrine signaling.
- Comorbidities significantly complicate the assessment and understanding of AKI progression.
Conclusions:
- Understanding the intricate mechanisms of AKI and its repair is crucial for improved patient outcomes.
- Further research integrating preclinical and clinical data is needed to address the challenges posed by comorbidities.
- The review highlights the complex nature of kidney injury and repair, emphasizing the need for a holistic approach.
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