Polyamine metabolism in ischemia reperfusion injury: common mitochondrial mechanisms and organ-specific differences

Abstract

Polyamines are essential polycations that play pivotal roles in various cellular processes, including cell proliferation, redox regulation, protein synthesis, and particularly the maintenance of mitochondrial function. During ischemia/reperfusion injury (I/RI), mitochondrial dysfunction emerges as a common mechanism underlying organ damage. This review systematically explores how polyamine metabolism regulates mitochondrial injury in I/RI, focusing on its impact on mitochondrial homeostasis and exacerbating organ damage through the modulation of reactive oxygen species, calcium homeostasis, mitochondrial membrane potential, and mitophagy. By analyzing polyamine metabolic alterations in the heart, kidney, liver, and brain during I/RI, we observe a common metabolic remodeling characterized by enhanced catabolism, while also identifying organ-specific regulatory responses. Finally, we summarize the potential intervention strategies targeting polyamine metabolism and discuss their translational prospects, offering new insights into therapeutic approaches for I/RI.