Lactate, a metabolic byproduct, has gained recognition as a highly influential signaling molecule. Lactylation, an emerging form of post-translational modification derived from lactate, plays a crucial role in numerous cellular processes such as inflammation, embryonic development, tumor proliferation, and metabolism. However, the precise molecular mechanisms through which lactylation governs these biological functions in both physiological and pathological contexts remain elusive. Hence, it is imperative to provide a comprehensive overview of lactylation in order to elucidate its significance in biological processes and establish a foundation for forthcoming investigations. This review aims to succinctly outline the process of lactylation modification and the characterization of protein lactylation across diverse organisms. Additionally, A summary of the regulatory mechanisms of lactylation in cellular processes and specific diseases is presented. Finally, this review concludes by delineating existing research gaps in lactylation and proposing primary directions for future investigations.

This review focuses on the mechanisms of cation–π interactions in high-performance polymeric materials, highlighting advances in mechanical enhancement, energy storage, adsorption, and responsiveness, with prospects in conductivity and catalysis.

Purpose: Skin radiation damage is a prevalent form of tissue injury encountered during radiotherapy, radiation accidents, and occupational exposure. The only clinically approved radioprotective agent, amifostine, is associated with numerous side effects, underscoring the urgent need for the development of safe and effective radioprotective agents. Natural products with reductive properties possess high antioxidant activity and biocompatibility, but their low bioavailability limits their radioprotective efficacy and clinical application. To address this, we utilized epigallocatechin gallate (EGCG) as a model compound and employed nanotechnology to enhance cellular uptake of natural compounds, thereby improving their free radical scavenging capabilities. Methods: EGCG nanoparticles (EGCG NPs) with robust intracellular reactive oxygen species (ROS) scavenging ability were prepared via self-assembly. The morphology, size distribution, and antioxidant capacity of EGCG NPs were characterized. Cytocompatibility, intracellular ROS levels and DNA damage, cell migration and immune response of EGCG NPs to macrophages were tested in vitro. The in vivo radiation protection and biocompatibility of EGCG NPs were assessed in murine model. Results: The EGCG NPs was successfully prepared and compared to free EGCG, EGCG NPs demonstrated better cellular uptake, significantly enhancing their biocompatibility, intracellular ROS scavenging capacity, and ability to mitigate DNA damage. Furthermore, EGCG NPs facilitated fibroblast proliferation and migration, while inhibiting the polarization of macrophages towards the M1 phenotype in vitro. In animal levels, EGCG NPs exhibited markedly improved radioprotective efficacy over free EGCG, effectively reducing skin edema and ulceration, alleviating pathological conditions such as interstitial edema, dermal fluid accumulation, and inflammatory infiltration, decreasing the duration of skin injury, and promoting wound healing. Conclusion: This work offers novel insights into the therapeutic application of EGCG NPs as a potential alternative for skin radioprotection and provides a powerful approach for developing radioprotective agents derived from natural products.

Fibroblast activation protein (FAP) is highly expressed in solid tumors and may be a potential diagnostic and therapeutic target in solid cancers. Linagliptin inhibits FAP; however, the interaction mechanism between linagliptin and FAP remains unclear. In this study, the binding free energy for linagliptin with human FAP was estimated at -13.66 kcal/mol, and the dissociation constant was 243 nM based on surface plasmon resonance analyses. E203, E204, and Y656 formed hydrogen bonds with ammonium. Y625 formed an unstable hydrogen bond with the carbonyl group. W623 and Y541 interacted with the quinazoline and pyrimidine-2,4-dione rings, respectively, via π-π interactions. The butyne group formed hydrophobic interactions with residues V650, Y653, Y656, and Y660. ZINC000299754517 and ZINC000299754576 were identified as potential FAP inhibitors. The R1 and R4 regions of linagliptin could be optimized to increase its FAP binding affinity. These findings can guide linagliptin structural optimization to improve its FAP binding affinity.

Nanosecond Pulsed Electric Fields (nsPEFs) treatment has demonstrated anti-tumor effects on various cancer cell lines. However, the use of this treatment in pancreatic cancer is limited. This study demonstrated that nsPEFs treatment effectively suppressed the proliferation and metastasis of pancreatic cancer cells, while also inducing DNA damage. Meanwhile, animal experiments have shown that nsPEFs effectively suppressed the growth of pancreatic cancer, even in cases where the tumor volume exceeded 500-600 mm³ at the initiation of treatment. Notably, a single treatment session was found to significantly inhibit tumor growth, while also showing no adverse effects on the main organs of the mice. RNA sequencing and bioinformatics revealed that seven key genes (CDK1, CENPA, UBE2C, CCNB2, PLK1, CCNA2, and CCNB14) were significantly correlated with the overall survival rate of patients with pancreatic cancer. Through the application of the competing endogenous RNA (ceRNA) hypothesis, two miRNAs (has-let-7b-5p and hsa-miR-193b-3p) and four lncRNAs (MIR4435-2HG, ZNF436-AS1, LINC01089, and MIR4435-2HG) were identified as significantly impacting the overall survival of pancreatic cancer patients. We have effectively developed an mRNA-miRNA-lncRNA network that has the potential to stimulate further investigation into the underlying mechanisms of nsPEFs on pancreatic cancer.