Nanomedicine-based approaches to protect cardiac tissue necrosis from ischemic events

Myocardial infarction (MI) is one of the leading causes of death worldwide, and there is an urgent need for novel therapeutic approaches to facilitate healing and reduce long-term adverse sequelae after MI, especially in high-risk groups such as elderly individuals. Current management primarily aims to restore blood flow and reduce acute myocardial damage through the use of thrombolytic agents, antiplatelet drugs, and invasive procedures. However, these treatments tend to treat symptoms rather than the cause-specifically, cardiomyocyte death and/or excessive inflammation that can degrade the heart-which is a direct route to heart failure. This review highlights emerging therapeutic approaches that focus on critical cellular events of myocardial repair, such as apoptosis, ferroptosis, pyroptosis, and autophagy. This discussion highlights the emergence of anti-apoptotic therapies that utilize nanoparticles for the targeted delivery of microRNAs and small molecule inhibitors, which are intended to preserve cardiomyocyte viability. Furthermore, the discussion highlights strategies for ferroptosis and pyroptosis inhibition, demonstrating their roles in reducing oxidative stress and inflammatory damage. Much emphasis is placed on autophagy as an important mechanism for cellular repair, degradation of damaged components, and increased cardiomyocyte survival. Additionally, we discuss the modulation of the inflammatory response via the use of reactive oxygen species (ROS) scavengers and anti-inflammatory agents to protect myocardial tissue. In all these therapeutic developments, nanotechnology has a considerable role, permitting targeted drug delivery and improving efficacy with reduced systemic side effects. Taken together, these new approaches may translate into meaningful improvements in the clinical outcomes of patients with MI. This review thus emphasizes the multifactorial nature of myocardial injury and highlights the potential of targeted therapies aimed at improving cardiac repair and function post-MI.