Crosstalk between mitochondrial quality control and novel programmed cell death in pulmonary diseases

Dysfunctional mitochondrial quality control (MQC) and dysregulated programmed cell death (PCD) are increasingly recognized as key drivers of pulmonary diseases. This review explores the intricate crosstalk between MQC mechanisms, encompassing mitochondrial biogenesis, dynamics, mitophagy, and mitocytosis, and novel PCD pathways such as pyroptosis, ferroptosis, necroptosis, PANoptosis, cuproptosis, and disulfidptosis. We highlight how mitochondrial dysfunction triggers PCD and how PCD exacerbates mitochondrial damage, creating a vicious cycle that amplifies lung injury and inflammation. Emerging therapeutic strategies targeting these interconnected pathways show promise in mitigating pulmonary diseases. However, challenges remain in understanding the context-dependent roles and translating preclinical findings into clinical applications. Further research is still needed to elucidate the precise regulatory mechanisms governing MQC and PCD, identify novel therapeutic targets, and develop biomarkers for early disease detection and prognosis. This review underscores the potential of targeting MQC and PCD as a therapeutic direction for pulmonary diseases, offering new insights into disease pathogenesis and treatment.