Wenwen Shi

Ischemia-reperfusion (I/R) injury describes the pathological process wherein tissue damage, initially caused by insufficient blood supply (ischemia), is exacerbated upon the restoration of blood flow (reperfusion). This phenomenon can lead to irreversible tissue damage and is commonly observed in contexts such as cardiac surgery and stroke, where blood supply is temporarily obstructed. During ischemic conditions, the anaerobic metabolism of tissues and organs results in compromised enzyme activity. Subsequent reperfusion exacerbates mitochondrial dysfunction, leading to increased oxidative stress and the accumulation of reactive oxygen species (ROS). This cascade ultimately triggers cell death through mechanisms such as autophagy and mitophagy. Autophagy constitutes a crucial catabolic mechanism within eukaryotic cells, facilitating the degradation and recycling of damaged, aged, or superfluous organelles and proteins via the lysosomal pathway. This process is essential for maintaining cellular homeostasis and adapting to diverse stress conditions. As a cellular self-degradation and clearance mechanism, autophagy exhibits a dualistic function: it can confer protection during the initial phases of cellular injury, yet potentially exacerbate damage in the later stages. This paper aims to elucidate the fundamental mechanisms of autophagy in I/R injury, highlighting its dual role in regulation and its effects on both organ-specific and systemic responses. By comprehending the dual mechanisms of autophagy and their implications for organ function, this study seeks to explore the potential for therapeutic interventions through the modulation of autophagy within clinical settings.

Data sharing not applicable to this article as no datasets were generated or analysed during the current study.

To address the critical challenge of reducing Platinum (Pt) consumption in proton exchange membrane fuel cells (PEMFCs), we demonstrate a dual-parameter engineering strategy that synergistically enhances Pt utilization in PEMFCs through coordinated optimization of carbon support structure and ionomer content. We first engineer carbon supports with tunable specific surface areas (SSA: 200–1050 m 2 /g), achieving precise control of Pt nanoparticle size from 3.26 nm (low SSA) to 1.76 nm (high SSA). Concurrently, we optimize the ionomer-to-carbon (I/C) ratios in catalyst layer (CL) fabrication, ranging from 0.1 to 1.1. We established a volcano-type dependence of Pt utilization on both carbon support SSA and I/C ratio, peaking at SSA of 550 m 2 /g and I/C ratio of 0.6 owing to the balance between Pt nanoparticle size and ionomer/carbon support-mediated transport limitations. This optimal dual-parameter configuration achieves peak utilization of 37 W/mg Pt , significantly exceeding previously reported values. Our dual-parameter optimization strategy provides a systematic investigation for maximizing Pt utilization in next-generation PEMFCs, offering valuable insights into the interfacial engineering of supported catalysts. • Tuning carbon surface area controls platinum size and ionomer distribution. • Proper ionomer-to-carbon ratio balances proton and gas transport pathways. • Platinum utilization shows volcano trend with support area and ionomer content. • Highest platinum utilization of 37 W/mg at 550 m 2 /g and ratio of 0.6.

Data sharing is not applicable to this article as no datasets were generated or analysed during the current study.