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Exploring Phosphatase and Tensin Homologue Deleted on Chromosome Ten (PTEN) as a Potential Therapeutic Target for

Mansi Jha1, Lokesh Kumar Bhatt1

  • 1Department of Pharmacology, SVKM's Dr. Bhanuben Nanavati College of Pharmacy, Vile Parle (W), Mumbai 400056, India.

ACS Pharmacology & Translational Science
|August 14, 2025
PubMed

Insights

Phosphatase and tensin homologue deleted on chromosome ten (PTEN) inhibits cardiac hypertrophy and heart failure by regulating the PI3K/AKT/mTOR pathway. Restoring PTEN function offers a promising therapeutic strategy for heart conditions.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Cellular Signaling

Background:

  • Cardiovascular diseases, particularly heart failure, are leading global causes of mortality.
  • Heart failure stems from impaired cardiac myocyte function, often due to cardiac hypertrophy.
  • Cardiac hypertrophy involves cardiomyocyte thickening and myocardial enlargement, impacting heart function.

Purpose of the Study:

  • To review the role of Phosphatase and tensin homologue deleted on chromosome ten (PTEN) in cardiac hypertrophy.
  • To explore novel interactions of PTEN with noncoding RNAs and proteins.
  • To discuss therapeutic strategies targeting PTEN for heart failure treatment.

Main Methods:

  • Literature review of PTEN's function in cardiac myocytes.
  • Analysis of signaling pathways, including PI3K/AKT/mTOR.
  • Examination of noncoding RNAs and protein interactions with PTEN.
  • Review of pharmacological agents affecting PTEN.

Main Results:

  • PTEN acts as a negative regulator of the PI3K/AKT/mTOR pathway, crucial for cardiomyocyte growth and survival.
  • Dysregulation of PTEN contributes to unchecked cardiomyocyte proliferation and cardiac hypertrophy.
  • PTEN's activity is modulated by noncoding RNAs and interacting proteins.
  • Pharmacological restoration of PTEN expression and function shows therapeutic potential.

Conclusions:

  • PTEN plays a critical role in preventing cardiac hypertrophy and mitigating heart failure risk.
  • Targeting PTEN, through modulation of its interactions or pharmacological agents, represents a viable therapeutic avenue.
  • Further research into PTEN-modulating therapies could lead to effective treatments for heart failure.

Keywords:
PI3K/AKT/mTOR signalingPTENcardiac hypertrophyheart failuretherapeutics

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