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Numerous studies reported about potential effects of L-carnosine in regulation of tumor growth and metabolism. We evaluated the effects of different concentrations of L-carnosine from supplement on mitochondrial respiratory chain complexes of human embryo lung fibroblasts (MRC-5) and human breast cancer cells (MCF-7), with different energy pathways. Also, we analyzed the proliferation index and expression of various markers of oxidative stress.

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Cell-membrane targeting sonodynamic therapy combination with FSP1 inhibition for ferroptosis-boosted immunotherapy.

Mater Today Bio

February 2025

Breast Center, Department of General Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, PR China.

Cell membrane targeting sonodynamic therapy could induce the accumulation of lipid peroxidation (LPO), drive ferroptosis, and further enhances immunogenic cell death (ICD) effects. However, ferroptosis is restrained by the ferroptosis suppressor protein 1 (FSP1) at the plasma membrane, which can catalyze the regeneration of ubiquinone (CoQ10) by using NAD(P)H to suppress the LPO accumulation. This work describes the construction of US-active nanoparticles (TiF NPs), which combinate cell-membrane targeting sonosensitizer TBT-CQi with FSP1 inhibitor (iFSP1), facilitating cell-membrane targeting sonodynamic-triggered ferroptosis.

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Introduction: Coenzyme Q10 (CoQ10) is a fat-soluble vitamin-like quinone. The plasma levels of CoQ10 are reduced in patients with chronic kidney disease (CKD). CoQ10 supplementation can improve mitochondrial function and decrease oxidative stress in these patients.

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Background: Coenzyme Q10 (CoQ10) nephropathy is a well-known cause of hereditary steroid-resistant nephrotic syndrome, primarily impacting podocytes. This study aimed to elucidate variations in individual cell-level gene expression in CoQ10 nephropathy using single-cell transcriptomics.

Methods: We conducted single-cell sequencing of a kidney biopsy specimen from a 5-year-old boy diagnosed with a CoQ10 nephropathy caused by a compound heterozygous COQ2 mutation complicated with immune complex-mediated glomerulonephritis.

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One of the underlying mechanisms of epilepsy (EP), a brain disease characterized by recurrent seizures, is considered to be cell death. Disulfidptosis, a proposed novel cell death mechanism, is thought to play a part in the pathogenesis of epilepsy, but the exact role is unclear. The gene expression omnibus series (GSE) 33000 and GSE63808 datasets were used to search for differentially expressed disulfidptosis-related molecules (DE-DRMs).

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