PTEN in kidney diseases: a potential therapeutic target in preventing AKI-to-CKD transition

Area of Science:

• Nephrology
• Molecular Biology
• Pathology

Background:

• Renal fibrosis drives chronic kidney disease (CKD) development, often stemming from acute kidney injury (AKI).
• Phosphatase and tensin homolog (PTEN) regulates renal cell function and homeostasis, impacting processes like apoptosis and fibrosis.
• The precise role of PTEN in AKI and subsequent maladaptive repair remains incompletely understood.

Purpose of the Study:

• To review the multifaceted role of PTEN in renal pathology during AKI and CKD.
• To elucidate the mechanisms underlying PTEN's influence on kidney injury and repair.
• To summarize potential therapeutic strategies targeting PTEN for AKI and CKD.

Main Methods:

• Literature review of studies investigating PTEN in renal injury models.
• Analysis of PTEN's involvement in cellular processes like oxidative stress and autophagy.
• Examination of PTEN's role in immune cell modulation and fibrosis.

Main Results:

• PTEN significantly influences cell proliferation, apoptosis, and mitochondrial metabolism during the AKI-to-CKD transition.
• PTEN's activity is implicated in oxidative stress, autophagy, and immune cell recruitment in kidney injury.
• Modulation of PTEN impacts renal fibrosis progression.

Conclusions:

• PTEN plays a critical, complex role in the pathogenesis of AKI and CKD.
• Understanding PTEN's mechanisms offers insights into kidney disease progression.
• Targeting PTEN presents a promising avenue for developing novel therapies for kidney diseases.