Trackins (Trk-Targeting Drugs): A Novel Therapy for Different Diseases
Many routes may lead to the transition from a healthy to a diseased phenotype. However, there are not so many routes to travel in the opposite direction; that is, therapy for different diseases. The following pressing question thus remains: what are the pathogenic routes and how can be they countera...
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| Main Authors: | , , , , , , , , |
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| Format: | Book |
| Published: |
MDPI AG,
2024-07-01T00:00:00Z.
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| Summary: | Many routes may lead to the transition from a healthy to a diseased phenotype. However, there are not so many routes to travel in the opposite direction; that is, therapy for different diseases. The following pressing question thus remains: what are the pathogenic routes and how can be they counteracted for therapeutic purposes? Human cells contain >500 protein kinases and nearly 200 protein phosphatases, acting on thousands of proteins, including cell growth factors. We herein discuss neurotrophins with pathogenic or metabotrophic abilities, particularly brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), pro-NGF, neurotrophin-3 (NT-3), and their receptor Trk (tyrosine receptor kinase; pronounced "track"). Indeed, we introduced the word <i>trackins</i>, standing for Trk-targeting drugs, that play an agonistic or antagonistic role in the function of TrkB<sup>BDNF</sup>, TrkC<sup>NT−3</sup>, TrkA<sup>NGF</sup>, and TrkA<sup>pro-NGF</sup> receptors. Based on our own published results, supported by those of other authors, we aim to update and enlarge our <i>trackins concept</i>, focusing on (1) agonistic trackins as possible drugs for (1a) neurotrophin-deficiency cardiometabolic disorders (hypertension, atherosclerosis, type 2 diabetes mellitus, metabolic syndrome, obesity, diabetic erectile dysfunction and atrial fibrillation) and (1b) neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, and multiple sclerosis), and (2) antagonistic trackins, particularly TrkA<sup>NGF</sup> inhibitors for prostate and breast cancer, pain, and arrhythmogenic right-ventricular dysplasia. Altogether, the druggability of TrkA<sup>NGF</sup>, TrkA<sup>pro-NGF</sup>, TrkB<sup>BDNF</sup>, and TrkC<sup>NT−3</sup> receptors via trackins requires a further translational pursuit. This could provide rewards for our patients. |
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| Item Description: | 10.3390/ph17070961 1424-8247 |