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Channels and Transporters as Drug Targets
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Channels and Transporters as Drug Targets

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Chemical Biology".

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 5581

Special Issue Editors

Dr. Hongsheng Zhang

E-Mail Website
Guest Editor
Faculty of Environment and Life, Beijing University of Technology, Beijing 100124, China
Interests: drug targets; molecular pharmacology; biomarkers; redox; metabolism
Dr. Zhe Zhou

E-Mail Website
Guest Editor
Department of Bioinformatics, Beijing Institute of Microbiology and Epidemiology, Beijing 100071, China
Interests: drug targets; biomarkers; molecular pharmacology

Special Issue Information

Dear Colleagues,

As the guest editors of a timely, topical and high-quality collection titled “Channels and Transporters as Drug Targets” in Molecules, we are delighted to announce this exciting initiative, and we are particularly encouraging “Channels and Transporters as Drug Targets” in all areas of pharmacology and chemical biology around the world to take part. Channels and transporters typically consist of biomolecules that play key roles in a large variety of physiological and pathological processes. Importantly, many links to human diseases have been established, such as links to cardiovascular diseases, cancer, neurodegenerative diseases, immune diseases, infectious diseases or metabolic diseases, and channels and transporters as novel and promising therapeutic approaches for these diseases have been proposed. This collection will bring together the latest high-quality contributions to channels and transporters as drug targets.

The aim of this Special Issue is to publish original papers and reviews dealing with the recent developments in the field of channels and transporters as drug targets. We very much look forward to your contributions.

Dr. Hongsheng Zhang
Dr. Zhe Zhou
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Molecules is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • drug targets
  • channels
  • transporters
  • targeted therapy
  • pharmacology
  • novel therapy
  • biomarkers
  • prognostic marker
  • precision medicine
  • drug discovery

Published Papers (3 papers)

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Research

14 pages, 1591 KiB  
Article
Stretch-Induced Down-Regulation of HCN2 Suppresses Contractile Activity
by Job Baffin Kola, Botagoz Turarova, Dora Csige, Ádám Sipos, Luca Varga, Bence Gergely, Farah Al Refai, Iván P. Uray, Tibor Docsa and Karen Uray
Molecules 2023, 28(11), 4359; https://doi.org/10.3390/molecules28114359 - 26 May 2023
Viewed by 1104
Abstract
Although hyperpolarization-activated and cyclic nucleotide-gated 2 channels (HCN2) are expressed in multiple cell types in the gut, the role of HCN2 in intestinal motility is poorly understood. HCN2 is down-regulated in intestinal smooth muscle in a rodent model of ileus. Thus, the purpose [...] Read more.
Although hyperpolarization-activated and cyclic nucleotide-gated 2 channels (HCN2) are expressed in multiple cell types in the gut, the role of HCN2 in intestinal motility is poorly understood. HCN2 is down-regulated in intestinal smooth muscle in a rodent model of ileus. Thus, the purpose of this study was to determine the effects of HCN inhibition on intestinal motility. HCN inhibition with ZD7288 or zatebradine significantly suppressed both spontaneous and agonist-induced contractile activity in the small intestine in a dose-dependent and tetrodotoxin-independent manner. HCN inhibition significantly suppressed intestinal tone but not contractile amplitude. The calcium sensitivity of contractile activity was significantly suppressed by HCN inhibition. Inflammatory mediators did not affect the suppression of intestinal contractile activity by HCN inhibition but increased stretch of the intestinal tissue partially attenuated the effects of HCN inhibition on agonist-induced intestinal contractile activity. HCN2 protein and mRNA levels in intestinal smooth muscle tissue were significantly down-regulated by increased mechanical stretch compared to unstretched tissue. Increased cyclical stretch down-regulated HCN2 protein and mRNA levels in primary human intestinal smooth muscle cells and macrophages. Overall, our results suggest that decreased HCN2 expression induced by mechanical signals, such as intestinal wall distension or edema development, may contribute to the development of ileus. Full article
(This article belongs to the Special Issue Channels and Transporters as Drug Targets)
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19 pages, 2861 KiB  
Article
Resveratrol, a New Allosteric Effector of Hemoglobin, Enhances Oxygen Supply Efficiency and Improves Adaption to Acute Severe Hypoxia
by Zongtang Chu, Weidan Li, Guoxing You, Yuzhi Chen, Dong Qin, Peilin Shu, Yujing Wang, Ying Wang, Lian Zhao and Hong Zhou
Molecules 2023, 28(5), 2050; https://doi.org/10.3390/molecules28052050 - 22 Feb 2023
Viewed by 2152
Abstract
Acute altitude hypoxia represents the cause of multiple adverse consequences. Current treatments are limited by side effects. Recent studies have shown the protective effects of resveratrol (RSV), but the mechanism remains unknown. To address this, the effects of RSV on the structure and [...] Read more.
Acute altitude hypoxia represents the cause of multiple adverse consequences. Current treatments are limited by side effects. Recent studies have shown the protective effects of resveratrol (RSV), but the mechanism remains unknown. To address this, the effects of RSV on the structure and function of hemoglobin of adult (HbA) were preliminarily analyzed using surface plasmon resonance (SPR) and oxygen dissociation assays (ODA). Molecular docking was conducted to specifically analyze the binding regions between RSV and HbA. The thermal stability was characterized to further validate the authenticity and effect of binding. Changes in the oxygen supply efficiency of HbA and rat RBCs incubated with RSV were detected ex vivo. The effect of RSV on the anti-hypoxic capacity under acute hypoxic conditions in vivo was evaluated. We found that RSV binds to the heme region of HbA following a concentration gradient and affects the structural stability and rate of oxygen release of HbA. RSV enhances the oxygen supply efficiency of HbA and rat RBCs ex vivo. RSV prolongs the tolerance times of mice suffering from acute asphyxia. By enhancing the oxygen supply efficiency, it alleviates the detrimental effects of acute severe hypoxia. In conclusion, RSV binds to HbA and regulates its conformation, which enhances oxygen supply efficiency and improves adaption to acute severe hypoxia. Full article
(This article belongs to the Special Issue Channels and Transporters as Drug Targets)
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13 pages, 4847 KiB  
Article
The miRNA-185-5p/STIM1 Axis Regulates the Invasiveness of Nasopharyngeal Carcinoma Cell Lines by Modulating EGFR Activation-Stimulated Switch from E- to N-Cadherin
by Yue Luo, Jiaxiang Ye, Yayan Deng, Yujuan Huang, Xue Liu, Qian He, Yong Chen, Qiuyun Li, Yan Lin, Rong Liang, Yongqiang Li, Jiazhang Wei and Jinyan Zhang
Molecules 2023, 28(2), 818; https://doi.org/10.3390/molecules28020818 - 13 Jan 2023
Cited by 3 | Viewed by 1643
Abstract
Distant metastasis remains the primary cause of treatment failure and suggests a poor prognosis in nasopharyngeal carcinoma (NPC). Epithelial-mesenchymal transition (EMT) is a critical cellular process for initiating a tumor invasion and remote metastasis. Our previous study showed that the blockage of the [...] Read more.
Distant metastasis remains the primary cause of treatment failure and suggests a poor prognosis in nasopharyngeal carcinoma (NPC). Epithelial-mesenchymal transition (EMT) is a critical cellular process for initiating a tumor invasion and remote metastasis. Our previous study showed that the blockage of the stromal interaction molecule 1 (STIM1)-mediated Ca2+ signaling blunts the Epstein–Barr virus (EBV)-promoted cell migration and inhibits the dissemination and lymphatic metastasis of NPC cells. However, the upstream signaling pathway that regulates the STIM1 expression remains unknown. In this follow-up study, we demonstrated that the miRNA-185-5p/STIM1 axis is implicated in the regulation of the metastatic potential of 5–8F cells, a highly invasive NPC cell line. We demonstrate that the knockdown of STIM1 attenuates the migration ability of 5–8F cells by inhibiting the epidermal growth factor receptor (EGFR) phosphorylation-induced switch from E- to N-cadherin in vitro. In addition, the STIM1 knockdown inhibited the locoregional lymphatic invasion of the 5–8F cells in mice. Furthermore, we identified miRNA-185-5p as an upstream regulator that negatively regulates the expression of STIM1. Our findings suggest that the miRNA-185-5p/STIM1 axis regulates the invasiveness of NPC cell lines by affecting the EGFR activation-modulated cell adhesiveness. The miRNA-185-5p/STIM1 axis may serve as a potentially effective therapeutic target for the treatment of NPC. Full article
(This article belongs to the Special Issue Channels and Transporters as Drug Targets)
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