CHCHD1 (Coiled-Coil-Helix-Coiled-Coil-Helix Domain Containing 1)

CHCHD1 expression correlated with Th2 cell infiltration (R = 0.57, p = 0.025) and programmed cell death 1 expression (p = 0.027). CHCHD1 promotes EMT and immune evasion in HCC via TGF-β1 signaling, implicating it as a promising biomarker and therapeutic target.

Clioquinol (10-50 μm) induced OMA1 mitochondrial protease-dependent degradation of the dynamin-related GTPase OPA1 and suppressed the expression of CHCHD10 and CHCHD2 involved in the maintenance of cristae structure. These results suggest that mitochondrial toxicity is one of the mechanisms of clioquinol-induced neuronal cell death.

The findings revealed that DNAJB9, CHCHD10, and suppressor of cytokine signaling 3 exhibited protective effects against GC, while Syntaxin-8, alcohol dehydrogenase 7, and UDP-glucose 4-epimerase were associated with increased GC risk at the genetic level. In the present study, the six plasma proteins identified through comprehensive MR analysis may serve as potential biomarkers for GC, offering new insights for future molecular diagnosis and therapeutic strategies.

57 drugs, including nelarabine and vorinostat, were predicted to interact with the prognostic genes. Seven genes (TRIAP1, TOMM7, PINK1, CHCHD10, PPIF, BCL2L1, NDUFA13) involved in mitochondrial function and PCD pathways were identified as prognostic markers in MM. These findings provide insights into MM biology and prognosis, highlighting potential therapeutic targets.

In these cells, transient elevation of cytoplasmic Ca2+ facilitated the activation of calpain and caspase-3, accompanied by the processing and insolubilization of TDP-43. These observations suggest that CHCHD2 P14L causes abnormal Ca2+ dynamics and TDP-43 aggregation, reflecting the pathophysiology of ALS.

In contrast, the overexpression of CHCHD10 alleviated infection-induced detrimental effect in mitochondrial fusion, thereby impeding viral proliferation. In summary, NDV enhances its replication by inhibiting the CHCHD10 protein, which impedes mitochondrial fusion and suppresses IFN-β production through the activation of IRF3 and NF-κB.

This study analyzed the tumor ecosystem of primary and metastatic UM, providing a metastasis-related model that could be used to evaluate the prognosis, risk of metastasis, immunotherapy, and efficacy of antineoplastic drug treatment of UM.

This review overviews the current evidence regarding neuroinflammatory markers in the ALS/FTD continuum, focusing on the neuroinflammatory pathways involved in the genetic cases, moving from post-mortem reports to in vivo biofluid and neuroimaging data. We further discuss the potential link between genetic and autoimmune disorders and potential therapeutic implications.