Kidney is a highly energy-demanding organ rich in mitochondria. Numerous studies have indicated that mitochondria play a crucial role in maintaining normal kidney function and in the pathogenesis of various kidney diseases. Mitochondrial DNA is the exclusive genome of mitochondria. Damage to mtDNA not only leads to mitochondrial dysfunction and degradation of mitochondrial quality, but also acts as an endogenous inflammatory molecule, activating various inflammatory pathways, which contribute to cellular damage and the progression of kidney diseases. This article reviews the mechanisms of mitochondrial DNA damage and its significant role in triggering inflammatory injury in kidney diseases. Additionally, it summarizes the current research progress on various intervention strategies targeting this type of damage.

The aim of this experiment is to investigate the mechanism of liver cell damage induced by nonylphenol(NP).After establishing an in vitro model of NP induced BRL-3A liver cell injury,changes of oxidative damage markers were evaluated,Fe2+content was determined,the ultrastruc-ture of BRL-3A was observed,and the expression level of iron death marker proteins were deter-mined.The results showed that NP could significantly increase ROS and MDA in BRL-3A cells(P＜0.05);the GSH content,GSH Px activity,and SOD activity were significantly reduced(P＜0.05);the Fe2+content significantly increased(P＜0.05)and showed a dose-dependent effect;the mitochondrial volume of BRL-3A cells significantly decreases,the mitochondrial cristae break or e-ven disappear,and some mitochondria show vacuolization;the expression levels of iron homeostasis related proteins TFR1 and FTH1 were significantly reduced(P＜0.05).The results indicate that ferroptosis is involved in the mechanism of NP induced liver cell damage,which bene-fits for further exploration of NP pathogenesis.