TRPV1 (Transient Receptor Potential Cation Channel Subfamily V Member 1)

Importantly, TRPV1 expression correlated positively with cancer stem cell markers in both murine models and human samples. Collectively, our results reveal that TRPV1 is not only overexpressed in PCa but also contributes to proliferation regulation and stemness features, positioning it as a potential diagnostic and prognostic biomarker for prostate cancer.

Consequently, this regulatory cascade led to a significant decrease in pro-inflammatory cytokines, including Interleukin-1Beta (IL-1β), Interleukin-6 (IL-6), and Tumor Necrosis Factor-Alpha (TNF-α), and concurrently restored intestinal barrier function by upregulating the expression of Occludin and Mucin2 (Muc2). This study elucidates a protective role of VD3 in UC, whereby it coordinately regulates immune responses and barrier function via the TRPV1-MAPK signaling pathway, providing a novel theoretical and experimental foundation for VD3-based therapy for UC.

Structural and functional insights into these peptides reveal mechanisms underlying their target specificity and pharmacological advantages, such as blood-brain barrier penetration and low immunogenicity. This review underscores the originality of BmK peptides as molecular tools and lead compounds for next-generation neurology therapeutics, providing a focused resource for researchers in ion channel pharmacology and peptide-based drug design.

This "signal hijacking "paradigm recasts cancer as a battle for communicative control within the ecosystem. We thus propose that reestablishing system-wide signaling homeostasis, rather than pursuing pure cytoreduction, represents a fundamental strategy to overcome therapy resistance.

In addition, PI3K, AKT, and pAKT protein expressions were also reduced in both cell lines, indicating downregulation of PI3K/Akt signaling pathway. Phytochemicals in E. bicolor xylene extract could become promising ingredients for developing breast cancer therapeutics.

Our data also provide the first evidence of heat-induced activation of human TRPV2. Considering previous evidence for TRPV2 and TRPC5 expression in the oral cavity and their roles in oral pain and cancer, our findings indicate that these polymodal channels may participate not only in detecting specific astringent compounds, but also in mediating their broader health-related and anesthetic actions.

This study is the first to demonstrate that MOE alleviates respiratory inflammation and allergic asthma by targeting the TRPV1/NFAT/TSLP pathway, with honokiol preliminarily identified as its key bioactive component. These findings clarify the pharmacodynamic basis of MOE and propose a novel plant-derived candidate for asthma therapy.

Our study suggests that TRPV1 may be able to regulate the tumor microenvironment by regulating immune-related physiological activities and thereby regulating the occurrence and progression of cancers. Thus, TRPV1 could be used to develop new-targeted drugs for cancers.

UVA radiation increased the expression of G-protein-coupled receptors in melanoma cells (CB1/2/TRPV1/PPARγ), while the combined use of CBD/CBG reduced their expression. Therefore, the results have shown that CBD and CBG modulate the metabolism of phospholipids and PUFAs by altering the functions of melanoma cell membranes, potentially offering options for the use of these phytocannabinoids in the integrative biomedicine treatment of melanoma.

Western blot analysis further confirmed that KKP can effectively downregulate the expression of cytochrome P450 family 1 subfamily A member 1(CYP1A1), nitric oxide synthase 2(NOS2) and monoamine oxidase A(MAOA), arachidonate 5-lipoxygenase(ALOX5), prostaglandin-endoperoxide synthase 1(PTGS1), and p38 mitogen-activated protein kinase(p38 MAPK). In summary, the study reveals the clinical potential of KKP in the treatment of PIC and confirms that KKP alleviates inflammation and improves cough symptoms through multi-target and multi-pathway regulation, with the mechanism of action likely related to MAPK signaling pathway, arginine metabolism, and other inflammation-related pathways.

EA at ST36 produced significant analgesic and anti-inflammatory effects in IBS model rats. Visceral hypersensitivity was blunted and colonic inflammatory biomarkers (cytokines, TRPV1, NF-κB) were suppressed by EA, suggesting that EA at ST36 modulates neuro-immune pathways to relieve IBS-related pain. These findings support the therapeutic potential of ST36-targeted electroacupuncture for managing IBS visceral pain via inflammatory mechanism attenuation.

Here, we report that the pro-inflammatory disulfide isoform of high-mobility group box 1 (ds-HMGB1) is a key mediator of oxaliplatin-induced neuropathic pain, with DRG microglia-like tissue-resident macrophages (M-TRMφs) as its primary reservoir...M-TRMφ-derived ds-HMGB1 orchestrates neuropathic pain through pyroptotic release and TLR4/TRPV1 signaling in a redox-regulated macrophage-neuron axis in the DRG. ds-HMGB1 emerges as a potential biomarker and therapeutic target in CIPN.