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Last update 08 May 2025

TRPV2

Last update 08 May 2025

Basic Info

Synonyms

Osm-9-like TRP channel 2, OTRPC2, Transient receptor potential cation channel subfamily V member 2

+ [6]

Introduction

Calcium-permeable, non-selective cation channel with an outward rectification. Seems to be regulated, at least in part, by IGF1, PDGF and neuropeptide head activator. May transduce physical stimuli in mast cells. Activated by temperatures higher than 52 degrees Celsius; is not activated by vanilloids and acidic pH.

Drugs associated with TRPV2

CN119816492

Patent Mining

Target

TRPV2

Mechanism-

Active Org.

Ramot at Tel Aviv University Ltd.

Originator Org.

Ramot at Tel Aviv University Ltd.

Active Indication

Cardiovascular Diseases [+3]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

HG-1249

Target

TRPV1 x TRPV2

Mechanism

TRPV1 modulators [+1]

Active Org.-

Originator Org.

Human Genome Sciences, Inc.

Active Indication-

Inactive Indication

Nervous System Diseases

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with TRPV2

100 Translational Medicine associated with TRPV2

0 Patents (Medical) associated with TRPV2

645

Literatures (Medical) associated with TRPV2

01 Apr 2025·Advanced Science

Dual‐Gating Strategy: Ultrasound Activation of TRPV2 Channels and Borate‐Glass‐Induced Calcium Overload for Tumor Suppression

Article

Author: Wang, Qian ; Huang, Yangguang ; Liao, Yun ; Liu, Chunyu ; Huang, Rongkun ; Liu, Xuanyong ; Ouyang, Liping ; Tan, Ji ; Wong, Wing Tak ; Pan, Haobo ; Zhu, Haihong

AbstractEffective and precise treatment of breast cancer, particularly with bone metastasis, remains a significant challenge. Here, a dual‐gating strategy combining locally delivered borate glass (BG) and ultrasound (US) is developed for the precise and effective inhibition of breast cancer by targeting transient receptor potential vanilloid 2 (TRPV2). The results demonstrate that after local delivery of BG to the solid tumor, US effectively triggers calcium overload by activating the overexpressed TRPV2 channels, leading to mitochondrial autophagy and apoptosis in breast cancer cells, thereby inhibiting tumor growth with high precision. These effects are validated in subcutaneous, orthotopic, and TRPV2‐overexpressing breast cancer mouse models. In the bone metastasis model, BG combined with US treatment simultaneously suppresses tumor growth and promotes bone regeneration. Overall, this dual‐gating strategy offers a safe and efficient approach for the precise treatment of cancers with high TRPV2 expression and provides new insights into the design and clinical translation of calcium‐overload‐based cancer therapies.

01 Mar 2025·Plant Physiology

GT1 and ZmHB13/VRL1 regulate flower sexual differentiation by modulating jasmonate biosynthesis and signaling in maize

Article

Author: Ou, Xiaotong ; Wang, Haiyang ; Liu, Defan ; Zhong, Zhuojun ; Zou, Chen ; Zhang, Guisen ; Lu, Yun ; He, Mengqi ; Wang, Pinle ; Yuan, Yateng ; Xu, Xin ; Zhang, Tianyu ; Kong, Dexin ; Li, Heying ; Li, Chunlian ; Liu, Qing ; Li, Yaoyao ; Lai, Xiaojun ; Yao, Minhao ; Shen, Jie

AbstractAs a typical monoecious plant, maize (Zea mays L.) produces unisexual male and female flowers comprising tassels and ears, respectively. However, the molecular mechanisms underlying unisexual flower development remain largely unclear. Here, we identify a pair of homeodomain-leucine zipper (HD-ZIP) transcription factors, Grassy tiller1 (GT1) and ZmHB13 (also termed VRS1-like1, VRL1), which act synergistically to control carpel development in maize. Mutations in GT1, but not ZmHB13/VRL1, cause defects in carpel abortion in the tassels, resulting in feminized tassels. The gt1 Zmhb13 double mutants show a notably more severe phenotype and a defect in the abortion of the lower floret in the ear spikelet, resulting in extra fertile flowers and seed setting. We demonstrate that GT1 and ZmHB13/VRL1 bind directly to the promoters of 2 jasmonate (JA) biosynthesis genes, ZmLOX3 and ZmOPR7, and upregulate their expression in the developing flowers. The application of methyl jasmonate (MeJA) rescues the feminized tassel phenotype of the gt1 Zmhb13 double mutants. Additionally, GT1 and ZmHB13/VRL1 interact with the key JA-pathway repressors ZmJAZ4 and ZmJAZ26, thus releasing the key JA-pathway activators ZmMYC2a and ZmMYC2b to activate the downstream JA signaling processes. Our findings indicate that GT1 and ZmHB13/VRL1 function synergistically to regulate maize carpel development through modulating JA biosynthesis and signaling.

01 Feb 2025·Journal of Ethnopharmacology

Qisheng wan decoction alleviates the inflammation of CCI rats via TRP channels

Article

Author: Xiang, Chunxiao ; Li, Zaiqi ; Wei, Guihua ; Wang, Haoyan ; Wu, Yating ; Yan, Zhiyong ; Li, Xi

ETHNOPHARMACOLOGICAL RELEVANCEQisheng wan decoction (QWD), a traditional Chinese medicine, has promising potential anti-inflammatory effects against neuropathic pain (NP). However, its valid ingredients and specific anti-inflammatory mechanisms are still unclear.AIM OF THE STUDYThis study aimed to identify the active ingredients of QWD responsible for its anti-inflammatory effect by combining liquid chromatography with network pharmacology, and to explore its anti-inflammatory mechanism by chronic constriction injury (CCI) model rats.MATERIALS AND METHODSThe UHPLC-Q Exactive Orbitrap-MS technique was used to identify the active ingredients of QWD. The potential ingredients of QWD, which targeted to the pathways of treating NP, were performed by network pharmacology, molecular docking and molecular dynamics simulations. After CCI rats-induced NP model operation, QWD (5.6 g/kg/d, 11.2 g/kg/d, 22.4 g/kg/d) and Pregabalin (10 g/kg/d) as positive controls, were administered to the rats for 7 days. The behaviors of the different groups were tested at 0, 1, 3, 5, 7, 12 days, respectively. And the inflammatory factor including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) was detected by ELISA. Meantime, the inflammation of the sciatic nerve was evaluated by the hematoxylin-eosin staining. Ionized calcium-binding adapter molecule-1 (Iba-1) and glial fibrillary acidic protein (GFAP) were detected by immunohistochemistry. Moreover, the expressions of TRPA1, TRPV1, TRPV2, TRPV3, TRPV4, TRPM8, and P38 mitogen-activated protein kinase (MAPK) were tested by RT-PCR, Western blot, and immunohistochemistry.RESULTSAfter screening by the liquid chromatography and network pharmacology approach, seventy ingredients of QWD were identified, and seven core targets including oncogene tyrosine-protein kinase (SRC), mitogen-activated protein kinase 3 (MAPK3), signal transducer and activator of transcription 1 (STAT1), protein-serine-threonine kinase 1 (AKT1), mitogen-activated protein kinase 1 (MAPK1), TNF-α, and IL-6 were confirmed. Six active ingredients exhibited binding energies less than -5 kcal/mol, and the complexes were structurally stable within 50 ns. Pathway analysis indicated that transient receptor potential (TRP) channels were mainly responsible for anti-inflammatory mediator regulation. Compared with the CCI group, the behavioral tests showed that QWD-L, QWD-M, and QWD-H group alleviated mechanical, thermal and cold hyperalgesia (p < 0.05). HE staining results found out QWD-L, QWD-M, and QWD-H group decreased the inflammation of the sciatic nerve (p < 0.05). Similarly, compared with the CCI group, the serum level of TNF-α and IL-6 of QWD groups decreased conformably (p < 0.05). This reduction was downtrend with the inhibition of Iba-1, GFAP, and the TRP channel signaling pathway and p38 MAPK.CONCLUSIONSThis study provides a primary investigation of the composition of QWD for its anti-inflammation effect and its molecular mechanism in CCI model rats. And this therapeutic efficacy of QWD was achieved by decreasing the inflammation. QWD also inhibited the level TNF-α and IL-6 and decreasing the activation of Iba-1 and GFAP in glia. And this anti-inflammation mechanism involved in inhibiting the TRPA1, TRPV1, TRPV2, TRPV4, and TRPM8 and p38 MAPK signaling pathways. These findings provide a scientific and theoretical basis for the prevention and treatment of NP with QWD.

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TRPV2

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