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Mechanisms such as cellular senescence, genomic instability, telomere attrition, mitochondrial dysfunction, epigenetic alterations, and loss of proteostasis all contribute to an aging phenotype (Tenchov et al 2024) and are considered hallmarks or biomarkers for aging

Metabolic remodeling in pulmonary artery smooth muscle cells (PASMCs) and pulmonary artery endothelial cells (PAECs), including enhanced glycolysis and mitochondrial dysfunction, provides the energy and material basis for abnormal proliferation of vascular cells (Li D

To address this discrepancy, we further investigated the effects of sulforaphane and rotenone treatments in the SH-SY5Y cell line

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