PINK1 (PTEN Induced Kinase 1)

Collectively, our findings demonstrate that NaF activates the PINK1/Parkin-mediated mitophagy pathway; however, incomplete autophagic degradation leads to mitochondrial dysfunction and neuronal apoptosis, contributing to developmental neurotoxicity. Importantly, melatonin mitigates these adverse effects, suggesting its potential as a therapeutic agent for preventing fluoride-induced neurodevelopmental impairment through modulation of the PINK1/Parkin signaling axis.

Notably, it also triggers mitophagy through PINK1/Parkin upregulation, offering dual mitochondrial-targeted cytotoxicity. These findings position [UDRu] as a next-generation Ru(II) complex with multitargeted action, holding significant promise for overcoming resistance in TNBC therapy.

Collectively, this study elucidates the molecular mechanism by which co-exposure to PFOA, PFBA, and NPs induces neurotoxicity via suppression of mitophagy. These findings identify a potential molecular target for the prevention and treatment of PFAS- and NPs-induced neurological injury and provide valuable theoretical and experimental evidence for evaluating the neurotoxic risks of mixed environmental pollutants.

The study findings confirm the presence of common abnormalities in autophagy in CD and CRC, with decreased macroautophagy and chaperone-mediated autophagy, with the compensatory activation of mitophagy. BECN1, PINK1, and LAMP2 expressions may have a diagnostic and therapeutic value in the context of chronic inflammation and colorectal carcinogenesis.

Our study uncovered PINK1 as both a predictor of the ICB response and a key mediator of immune evasion by promoting neutrophil infiltration. These results highlight that the therapeutic targeting of neutrophils may represent a viable strategy to overcome ICB resistance in HCC.

QX1 protects against SIMI by enhancing CaMK I-dependent mitophagy. These findings highlight QX1's therapeutic potential for sepsis-induced cardiomyopathy. However, these results were obtained from a single standardized batch of QX1, and validation across multiple batches prepared from plants collected under different conditions is necessary to confirm the reproducibility and robustness of these mechanisms.

Salidroside may inhibit iron death by activating the PINK 1 / Parkin signaling pathway and thereby reduce cerebral ischemia-reperfusion injury. Targeted regulation of this pathway may become an important strategy to interfere with CIRI.

PINK1 acts as a tumor suppressor in colorectal cancer by inhibiting proliferation and migration, promoting apoptosis, and remodeling the epigenetic landscape through altering histone modifications and enhancing chromatin accessibility.

Interestingly, KNG1 upregulation could effectively reverse the effect of PRP-Exos on the tumor necrosis factor-alpha and high mobility histone 1 levels, protein expression of p-PI3K/PI3K and p-AKT/AKT, and mitophagy-related markers in HL-induced RAW264.7 cells. In conclusion, PRP-Exos facilitated macrophage mitophagy in diabetic wound healing by targeting KNG1 via PI3K-AKT pathway.

In vivo xenograft models also show that ANT1 knockdown markedly inhibits tumor growth. In conclusion, ANT1 may play a critical role in CRC progression by regulating mitophagy, providing a basis for its potential as a therapeutic target.

These findings indicate that inhibition of GS enzyme activity enhances oxidative stress and mitophagy, thereby promoting radiosensitivity in HCC cells. This study provides new insights into the role of GS in overcoming radiotherapy resistance and highlights its potential as a therapeutic target to improve radiotherapeutic outcomes in HCC.

The present study revealed that RHOT1 drives the malignant phenotype of GC through regulation of mitochondrial quality control and induction of oxidative stress, providing a rationale for developing novel anti‑tumor strategies by targeting mitochondrial function. RHOT1 may serve as a biomarker for prognostic assessment and individualized treatment of GC.