FABP1 (Fatty Acid Binding Protein 1)

This study uncovers a previously unrecognized role for BPCs in UC pathogenesis, highlighting their spatial dysfunction and potential as a therapeutic target. The identified FABP1-led matrix offers new insights into epithelial dysregulation in UC and its progression to colorectal cancer, suggesting that restoring BPC function may provide novel treatment avenues.

Our findings identify the FABP1/PPARγ axis as a central regulator of peroxisome-centered FAO and redox buffering in cetuximab-tolerant DTP cells. Targeting FABP1 collapses this adaptive metabolic-redox program, restores vulnerability to oxidative stress, and alleviates immune suppression, highlighting peroxisomal lipid metabolism as a therapeutically actionable vulnerability in refractory HNSCC.

Third, it integrates translational insights rarely synthesized in prior work: mapping natural compounds (icariin II and artesunate), repurposed drugs (sorafenib and melatonin), and novel modulators to disease stages (e.g., Lip-1 for fibrosis and salinomycin for RCC stem cells); highlighting strategies to reverse ferroptosis-related drug resistance (targeting DPP9 in RCC); and identifying ferroptosis-related genes (ACSL4 and PDIA4) as prognostic biomarkers. This review not only synthesizes ferroptosis pathophysiology and research advances but also delineates disease-tailored therapeutic strategies. By addressing key knowledge gaps-crosstalk between ferroptosis and other cell death modalities (e.g., pyroptosis), lack of kidney-specific clinical biomarkers, and underexplored roles in autoimmune nephritides-it provides a conceptual roadmap for mechanism-based diagnostics, precision therapeutics, and rational drug combinations, transcending traditional disease boundaries to advance clinical translation for both primary and secondary kidney diseases.

Macrophage depletion abrogates metastasis, while the FABP1 inhibitor orlistat reverses SPP1 upregulation in macrophages...Importantly, virtual screening identifies indole-3-acetic acid (IAA) as an RNF32 inhibitor that suppresses liver metastasis and reverses immunosuppression in vivo. This study establishes RNF32 as a dual-functional driver of metastasis and proposes IAA as a promising therapeutic agent, offering new hope for targeting both tumor-intrinsic EMT and the immune microenvironment in CRC liver metastasis.

Among them, the OSTP protein level in proteomics data and the mRNA level of the gene spp1 in TCGA database both showed an upward trend with the progression of the disease, suggesting that it may serve as a diagnostic and prognostic marker in plasma to reflect the disease progression of CRC patients. ROC analysis showed robust predictive performance, and PRM validation cohort correlated well with DIA results, providing potential insights for CRC research.

These results imply that PLA2G16-mediated C24:4 (n-6) accumulation in the lung acts as a metabolic disorder to CD8+ T cell antitumor activity and highlights a critical role of PLA2G16 in promoting TNBC lung metastasis. Targeting PLA2G16 and combination with anti-PD-1-based immunotherapy may be an effective strategy for clinical tumor immunotherapy.

Our study reveals a distinct lipid signature in gastric metaplasia characterized by TG and LD accumulation, providing novel therapeutic insights into targeting lipid metabolism to prevent GIM malignant transformation and reduce cancer risk.

Hepatocyte-specific FABP4 deletion does not alter hepatic fat accumulation in response to EtOH feeding. Hepatic FABP4 protein produced in response to EtOH is released from hepatocytes and exogenous FABP4 promotes hepatoma cell proliferation in vitro, an effect not observed for FABP5.

These mechanisms collectively enable H. pylori to propel gastric carcinogenesis, highlighting metabolism-targeted interventions as future solutions. This review summarizes how H. pylori remodel the gastric microenvironment and drives pathogenesis by manipulating host lipid, glucose, lactate, and amino acid metabolism.

While no significant differences in L-FABP levels were found between patients with and without infectious biliary or vascular complications (all p > 0.05), we proved a strong negative correlation between intraoperative blood transfusion volume and L-FABP levels on POD 5 (ρ = -0.677, p < 0.001) and POD 7 (ρ = -0.455, p = 0.025). Our findings suggest that L-FABP holds promise as a biomarker for the early detection of subclinical hepatic graft cellular injury, which is not detected by means of conventional biomarkers for liver function.

Riz1 knockout mice (KO) were randomly treated with either the AKT inhibitor afuresertib or the mTOR inhibitor rapamycin. Mice treated with the inhibitors exhibited significantly suppressed AKT/mTOR signaling pathway in liver, muscle, and adipose tissues, as well as downregulation of genes associated with energy and lipid metabolism (L-Fabp, Pparα/γ, Ubiad1, Cyp4a12). These findings demonstrate that inhibition of either the AKT or mTOR molecules mitigates obesity and metabolic dysregulation in Riz1-/- mice, highlighting the critical role of the RIZ1/AKT/mTOR axis in maintaining metabolic homeostasis.

These collective results indicate that exemestane induces hepatotoxicity in zebrafish primarily through activation of the p53 signaling pathway. This study provides valuable insights into the potential hepatotoxic effects of exemestane, offering important references for its clinical safety evaluation.