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Bilateral Renal Ischemia-Reperfusion Model for Acute Kidney Injury in Mice
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Molecular Mechanisms of Kidney Injury and Repair

Sandra Rayego-Mateos1,2, Laura Marquez-Expósito1,2, Raquel Rodrigues-Diez3,4

  • 1Cellular Biology in Renal Diseases Laboratory, IIS-Fundación Jiménez Díaz, Universidad Autónoma Madrid, 28040 Madrid, Spain.

International Journal of Molecular Sciences
|February 15, 2022
PubMed

Insights

Chronic kidney disease (CKD) and acute kidney injury (AKI) involve impaired kidney repair. Understanding cellular and molecular mechanisms offers new therapeutic targets for kidney regeneration and treating AKI-to-CKD transition.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Regenerative Medicine

Background:

  • Chronic kidney disease (CKD) is a growing global health concern, projected to be the fifth leading cause of death by 2040.
  • Acute kidney injury (AKI) exacerbates CKD progression, indicating a failure in kidney repair mechanisms.
  • Current treatments for CKD only slow progression and cannot effectively treat AKI or promote kidney regeneration.

Purpose of the Study:

  • To review the molecular and cellular mechanisms underlying kidney injury and repair.
  • To explore the AKI-to-CKD transition and identify factors contributing to dysfunctional repair.
  • To highlight potential therapeutic targets for enhancing kidney regeneration and recovery.

Main Methods:

  • Review of current literature on kidney injury, repair, and regeneration.
  • Focus on cellular events including macrophage roles, regulated cell death, senescence, polyploidization, and podocyte/parietal epithelial cell activation.
  • Discussion of therapeutic strategies targeting progenitor cells, stem cell secretomes, M2 macrophages, and senescent cell clearance.

Main Results:

  • The AKI-to-CKD transition is influenced by macrophages, necroinflammation, cellular senescence (SAPS), polyploidization, and epithelial cell activation.
  • Kidney repair involves resident renal progenitor cells, stem cells, specific macrophage phenotypes (M2), and clearance of senescent cells.
  • Dysfunctional repair mechanisms are key to CKD progression and AKI-to-CKD transition.

Conclusions:

  • Understanding the molecular intricacies of kidney injury and repair is crucial for developing novel biomarkers and therapeutics.
  • Targeting cellular senescence, macrophage phenotypes, and progenitor cell activity offers promising avenues for promoting kidney regeneration.
  • Effective interventions are needed to improve recovery from AKI and prevent the transition to CKD.
Keywords:
acute kidney injurycell deathchronic kidney diseasekidneymolecular mechanismsregenerationtreatment

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