TRPV4 (Transient Receptor Potential Cation Channel Subfamily V Member 4)

The study verified that GCM demonstrated potent anti-SARS-CoV-2 activity in both in vitro and in vivo models, effectively inhibiting viral replication while suppressing infection-induced cytokine storms. The results indicate that GCM is a highly promising anti-SARS-CoV-2 TCM monomer compound, which is worthy of further in-depth research and development.

TRPV4 expression was upregulated in Stages 3 OSF and 4 OSF and OSCC in the presence or absence of OSF compared to NOM and Stage 1 and 2 OSF. This study evaluates the unpaved role of TRPV4 in OSF, mediated by various canonical pathways, contributing to its development by increasing matrix-stiffness and rigidity, which further upregulates TRPV4 expression, ultimately facilitating carcinogenesis.

Overexpression of either Tet1 or TRPV4 rescued the KAT6A knockdown-induced osteoclast differentiation inhibition. KAT6A promotes osteoclast differentiation through a regulatory cascade involving Tet1-mediated TRPV4 upregulation, which identifying KAT6A as a potential therapeutic target for osteoporosis treatment.

Single-cell RNA sequencing demonstrated that CACNA1C was expressed in fibroblasts and myofibroblasts, PIEZO1 was expressed across all five cell subtypes, and TRPV4 was expressed in fibroblasts and monocytes or macrophages. This study initially identified unique molecular subtypes and key genes for patients with OC from the novel angle of MICs.

Furthermore, TRPV4 is downregulated by cisplatin in chemosensitive but not chemoresistant BLCA cells, underscoring its key role in bladder cancer chemoresistance. These findings position TRPV4 as a therapeutic target for enhancing BLCA treatment and overcoming drug resistance.

This MR analysis revealed a causal relationship between TRP and HCC, and MCOLN3 and TRPV4 were potential drug targets. They also served as potential molecular biomarkers for the efficacy of immunotherapy and/or targeted therapy, providing a strong theoretical basis for the clinical application of TRPs.

Moreover, Srsf3 KO suppresses the expression of ERα and Foxa genes to reduce Lifr and Egfr but induce Myc expression and promote liver cancer in female mice. Together, our data highlight a new functional paradigm of SRSF3 at its physiological level in tissue context-dependent gene regulation.

Furthermore, TRPV4 is downregulated by cisplatin in chemo-sensitive but not chemo-resistant BLCA cells, underscoring its key role in bladder cancer chemoresistance. These findings position TRPV4 as a therapeutic target for enhancing BLCA treatment and overcoming drug resistance.

Our results uncovered a novel mechanism of lymphatic contractile dysregulation mediated by the crosstalk between TRPV4-expressing myeloid cells, including LYVE1+ macrophages, and lymphatic muscle cells or lymphatic endothelial cells. These findings highlight potentially important roles of TRPV4 channels in lymphatic dysfunction associated with inflammation, including secondary lymphedema.

Schwann cell CM induced mechanical hypersensitivity in mice, which was blocked by pre-treatment with HC-067047. TRPV4 activation plays a role in mediating mechanically induced pain of oral cancer.

Notably, TRPV4 and IL-8 levels were significantly increased in the high-stiffness NPC tissues, and showed a positive correlation. Taken together, matrix stiffness promotes the malignant progression of NPC cells through the activation of the TRPV4/NOX4/IL-8 axis, which could be explored further as a potential target for NPC therapy.

TRPV4 is significantly upregulated in COAD and is associated with unfavorable patient outcomes. It appears to promote tumor progression by regulating the ferroptosis pathway, affecting the expression of key ferroptosis-related genes and proliferation markers. Targeting TRPV4 may offer a new therapeutic approach for COAD, and further research is warranted to explore its role in other cancers and to develop TRPV4-based therapies.