ALDH7A1 (Aldehyde Dehydrogenase 7 Family Member A1)

This multiomics study revealed that host metabolic genes linked to PPD are regulated through DNA methylation and metabolite-mediated host-microbiota interactions. These findings establish a foundation for future functional studies to develop mechanism-based therapeutic and preventive strategies targeting the gut-brain-metabolite axis in PPD.

Further drug virtual screening identified Dutasteride as a potential inhibitor of LPAR6. AGPAT3 is an important gene related to the prognosis of osteosarcoma. Its ability to modulate LPA signaling and TAM activity offers promising therapeutic opportunities for improving osteosarcoma treatment, particularly in immunotherapy contexts.

The increase in inflammasomes may promote EECs apoptosis and inhibit EECs invasion and migration. However, its in vivo inhibitory effects on endometriosis require further investigation.

As intravenous PLP is unfeasable for lifelong therapy, there is an urgent need for standardized, high-quality PLP preparations and exploration of alternative delivery routes such as intranasal administration. Regular hepatic monitoring should be implemented in all patients receiving chronic PLP therapy.

We demonstrate the first mammalian evidence that AASS inhibition is a viable strategy to rescue abnormal brain metabolism associated with PDE. This may target the intellectual disability and neurologic deficits caused by persistent lysine catabolic-related neurotoxicity despite adequate vitamin B6 supplementation.

In conclusion, Tan IIA sensitizes HCC cells to sublethal heat by targeting ALDH7A1, leading to disrupted glycolytic and osmolytic balance, subsequently hindering tumor cell survival and increasing apoptosis. These findings highlight a potentially novel strategy for preventing or treating recurrent HCC post-thermal ablation using Tan IIA with hyperosmotic reagents.

Our findings suggest a potential mechanistic link between PUFA metabolism and LC susceptibility, generating hypotheses that PUFA-associated pathways may modulate immune microenvironment characteristics. This computational study provides preliminary insights into potential immunometabolic therapeutic strategies in laryngeal cancer that warrant experimental validation.

This study identifies NSUN2 as a critical regulator of TNBC progression through tRNAVal-CAC m5C modification and codon-biased translation of glycolysis-related mRNAs. Our findings reveal a novel NSUN2-tRNAVal-CAC axis that orchestrates metabolic reprogramming and translational control in TNBC, offering a promising prognostic biomarker and therapeutic target.

P=N/A, N=30, Completed, University Hospital, Angers | Recruiting --> Completed

In conclusion, the present study emphasized the relevance of propionate metabolism in OS and introduced a novel gene signature for clinical outcome prediction. Furthermore, the identified genes, ABAT and ALDH7A1, may hold promise as potential therapeutic targets.

Treatment with the antioxidant N-acetyl cysteine (NAC) partially restored metabolic gene expression, reinforcing GSTP1's role in the interplay between redox regulation and metabolism in PDAC. By disrupting multiple metabolic pathways, GSTP1 depletion creates potential therapeutic vulnerabilities that could be targeted through metabolic and oxidative stress-inducing therapies to enhance treatment efficacy.

P=N/A, N=30, Recruiting, University Hospital, Angers | Not yet recruiting --> Recruiting | Trial primary completion date: Apr 2025 --> Sep 2025