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Household air pollution prevails in rural residences across China, yet a comprehensive nationwide comprehending of pollution levels and the attributable disease burdens remains lacking. This study conducted a systematic review focusing on elucidating the indoor concentrations of prevalent household air pollutants—specifically, PM2.5, PAHs, CO, SO 2 , and formaldehyde—in rural Chinese households. Subsequently, the premature deaths and economic losses attributable to household air pollution among the rural population of China were quantified through dose-response relationships and the value of statistical life. The findings reveal that rural indoor air pollution levels frequently exceed China's national standards, exhibiting notable spatial disparities. The estimated annual premature mortality attributable to household air pollution in rural China amounts to 966 thousand (95% CI: 714–1226) deaths between 2000 and 2022, representing approximately 22.2% (95% CI: 16.4%−28.1%) of total mortality among rural Chinese residents. Furthermore, the economic toll associated with these premature deaths is estimated at 486 billion CNY (95% CI: 358–616) per annum, constituting 0.92% (95% CI: 0.68%−1.16%) of China's GDP. The findings quantitatively demonstrate the substantial disease burden attributable to household air pollution in rural China, which highlights the pressing imperative for targeted, region-specific interventions to ameliorate this pressing public health concern. [Display omitted] • Indoor air pollution level in rural China was analyzed via a literature review. • Exposure to the pollutant exhibits heterogeneity across different spatial region. • Concerned air pollution attributes to 966 thousand premature deaths annually. • PM2.5 and CVD are key pollutant and disease contributing to health effects. • Targeted regional policies are needed to control rural household air pollution. [ABSTRACT FROM AUTHOR]

[Display omitted] Tumor cells with damaged mitochondria undergo metabolic reprogramming, but gene therapy targeting mitochondria has not been comprehensively reported. In this study, plasmids targeting the normal hepatocyte cell line (L-O2) and hepatocellular carcinoma cell line were generated using three genes SIRT3 , SIRT4 , and SIRT5. These deacetylases play a variety of regulatory roles in cancer and are related to mitochondrial function. Compared with L-O2, SIRT3 and SIRT4 significantly ameliorated mitochondrial damage in HCCLM3, Hep3B and HepG2 cell lines and regulated mitochondrial biogenesis and mitophagy, respectively. We constructed double-gene plasmid for co-express SIRT3 and SIRT4 using the internal ribosome entry site (IRES). The results indicated that the double-gene plasmid effectively expressed SIRT3 and SIRT4, significantly improved mitochondrial quality and function, and reduced mtDNA level and oxidative stress in HCC cells. MitoTracker analysis revealed that the mitochondrial network was restored. The proliferation, migration capabilities of HCC cells were reduced, whereas their differentiation abilities were enhanced. This study demonstrated that the use of IRES-linked SIRT3 and SIRT4 double-gene vectors induced the differentiation of HCC cells and inhibited their development by ameliorating mitochondrial dysfunction. This intervention helped reverse metabolic reprogramming, and may provide a groundbreaking new framework for HCC treatment. [ABSTRACT FROM AUTHOR]