AMPK activation; a potential strategy to mitigate TKI-induced cardiovascular toxicity

Arch Physiol Biochem. 2025 Jun;131(3):329-341. doi: 10.1080/13813455.2024.2426494. Epub 2024 Nov 11.

Abstract

The introduction of Tyrosine Kinase Inhibitors (TKIs) has revolutionised cancer treatment, yet concerns regarding cardiovascular toxicity have surfaced. This piece delves into the interplay between AMP-activated protein kinase (AMPK) signalling and TKI-induced cardiovascular toxicity. The study unravels the intricate relationship between AMPK activation and TKI-induced cardiovascular toxicity, aiming to ascertain whether AMPK can play a strategic role in mitigating adverse effects. Beyond unravelling mechanistic insights, the research sets the stage for future therapeutic approaches, envisioning AMPK activation as a pivotal connection for balancing effective cancer treatment with cardiovascular well-being. As research advances, the potential of AMPK activation not only addresses challenges in TKI-induced cardiovascular toxicity but also shapes the future landscape of personalised anticancer therapies. The article explores the mechanisms of TKI-induced toxicity, AMPK's impact on cardiovascular health, and the potential therapeutic implications of AMPK activation in alleviating TKI-associated toxicities.

Keywords: AMPK; Nrf2; SIRT1; cardiovascular toxicity; tyrosine kinase inhibitors.

Publication types

  • Review

MeSH terms

  • AMP-Activated Protein Kinases* / metabolism
  • Animals
  • Antineoplastic Agents* / adverse effects
  • Antineoplastic Agents* / therapeutic use
  • Cardiotoxicity* / etiology
  • Cardiotoxicity* / prevention & control
  • Cardiovascular Diseases* / chemically induced
  • Cardiovascular Diseases* / pathology
  • Cardiovascular Diseases* / prevention & control
  • Cardiovascular System* / drug effects
  • Enzyme Activation / drug effects
  • Humans
  • Neoplasms* / drug therapy
  • Protein Kinase Inhibitors* / adverse effects
  • Protein Kinase Inhibitors* / therapeutic use
  • Signal Transduction / drug effects

Substances

  • AMP-Activated Protein Kinases
  • Protein Kinase Inhibitors
  • Antineoplastic Agents