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Pharmaceuticals
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Potential Therapeutic Targets for the Treatment of Pathological Pain
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Potential Therapeutic Targets for the Treatment of Pathological Pain

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: 25 May 2025 | Viewed by 14411

Special Issue Editor

Dr. Sara Marchesan De Oliveira

E-Mail Website
Guest Editor
Graduate Program in Biological Sciences: Toxicological Biochemistry, Center of Natural and Exact Sciences, Federal University of Santa Maria, Camobi, Santa Maria 97105-900, RS, Brazil
Interests: kinins; cancer pathophysiology; adverse effects of chemotherapy; cancer pain; anticancer therapy-associated pain; drug delivery
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

As one of the most common reasons people seek medical care, pain is an issue of extreme relevance. Pathological pain, such as chronic inflammatory, neuropathic, and dysfunctional or nociplastic pain impairs the life quality of patients, leading to the development of anxiety, depression, labour capacity loss, and even distancing from family members and society. Often, the analgesic drugs used clinically present limited efficacy and cause various adverse effects, including analgesic tolerance, dependency, and abuse possibility, limiting their use. Thus, identifying potential therapeutic targets for treating pathological pain is highly relevant for developing more effective and safe analgesic drugs for adequate pain relief. This Special Issue is intended to investigate potential therapeutic targets for developing new analgesics, the signalling pathways involved in these processes, and the analgesic effect of synthetic drugs or natural products in pathological pain models.

We look forward to receiving your contributions.

Dr. Sara Marchesan De Oliveira
Guest Editor

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 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

  • analgesics
  • pathological pain models
  • inflammation
  • rheumatoid arthritis
  • neuropathy
  • nerve injuries
  • spinal cord injuries
  • antineoplastics
  • headaches
  • irritable bowel syndrome
  • fibromyalgia

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Published Papers (4 papers)

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Research

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30 pages, 13074 KiB  
Article
An Azomethine Derivative, BCS3, Targets XIAP and cIAP1/2 to Arrest Breast Cancer Progression Through MDM2-p53 and Bcl-2-Caspase Signaling Modulation
by Reetuparna Acharya, Pran Kishore Deb, Katharigatta N. Venugopala and Shakti Prasad Pattanayak
Pharmaceuticals 2024, 17(12), 1645; https://doi.org/10.3390/ph17121645 - 6 Dec 2024
Cited by 1 | Viewed by 1208
Abstract
Background: Breast cancer influences more than 2 million women worldwide annually. Since apoptotic dysregulation is a cancer hallmark, targeting apoptotic regulators encompasses strategic drug development for cancer therapy. One such class of apoptotic regulators is inhibitors of apoptosis proteins (IAP) which are [...] Read more.
Background: Breast cancer influences more than 2 million women worldwide annually. Since apoptotic dysregulation is a cancer hallmark, targeting apoptotic regulators encompasses strategic drug development for cancer therapy. One such class of apoptotic regulators is inhibitors of apoptosis proteins (IAP) which are a class of E3 ubiquitin ligases that actively function to support cancer growth and survival. Methods: The current study reports design, synthesis, docking analysis (based on binding to IAP-BIR3 domains), anti-proliferative and anti-tumor potential of the azomethine derivative, 1-(4-chlorophenyl)-N-(4-ethoxyphenyl)methanimine (BCS3) on breast cancer (in vitro and in vivo) and its possible mechanisms of action. Results: Strong selective cytotoxic activity was observed in MDA-MB-231, MCF-7, and MDA-MB-468 breast cancer cell lines that exhibited IC50 values, 1.554 µM, 5.979 µM, and 6.462 µM, respectively, without affecting normal breast cells, MCF-10A. For the evaluation of the cytotoxic potential of BCS3, immunofluorescence, immunoblotting, and FACS (apoptosis and cell cycle) analyses were conducted. BCS3 antagonized IAPs, thereby causing MDM2-p53 and Bcl-2-Caspase-mediated intrinsic and extrinsic apoptosis. It also modulated p53 expression causing p21-CDK1/cyclin B1-mediated cell cycle arrest at S and G2/M phases. The in vitro findings were consistent with in vivo findings as observed by reduced tumor volume and apoptosis initiation (TUNEL assay) by IAP downregulation. BCS3 also produced potent synergistic effects with doxorubicin on tumor inhibition. Conclusions: Having witnessed the profound anti-proliferative potential of BCS3, the possible adverse effects related to anti-cancer therapy were examined following OECD 407 guidelines which confirmed its systemic safety profile and well tolerability. The results indicate the promising effect of BCS3 as an IAP antagonist for breast cancer therapy with fewer adverse effects. Full article
(This article belongs to the Special Issue Potential Therapeutic Targets for the Treatment of Pathological Pain)
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18 pages, 5947 KiB  
Article
Kinin B2 Receptor Mediates Cisplatin-Induced Painful Peripheral Neuropathy by Intracellular Kinase Pathways and TRPA1 Channel Sensitisation
by Gabriela Becker, Maria Fernanda Pessano Fialho, Evelyne Silva Brum and Sara Marchesan Oliveira
Pharmaceuticals 2023, 16(7), 959; https://doi.org/10.3390/ph16070959 - 4 Jul 2023
Cited by 5 | Viewed by 1728
Abstract
Chemotherapy-induced peripheral neuropathy is a severe clinical problem frequently associated with cisplatin use. Although its pathophysiology is poorly understood, it is known that kinin receptors and the transient receptor potential ankyrin 1 (TRPA1) channel play a significant role in the peripheral neuropathy induced [...] Read more.
Chemotherapy-induced peripheral neuropathy is a severe clinical problem frequently associated with cisplatin use. Although its pathophysiology is poorly understood, it is known that kinin receptors and the transient receptor potential ankyrin 1 (TRPA1) channel play a significant role in the peripheral neuropathy induced by cisplatin in rodents. However, the role of signalling pathways downstream from B2 kinin receptors activation and sensitisation of the TRPA1 channel remains unknown in this model. The cisplatin-induced neuropathy model caused mechanical and cold allodynia in male Swiss mice. Antagonists for kinin B2 and B1 receptors and the TRPA1 channel attenuated the painful parameters. Local sub-nociceptive doses of kinin B2 receptor (bradykinin) and TRPA1 channel (allyl isothiocyanate; AITC) agonists enhanced the painful parameters in cisplatin-treated mice, which their respective antagonists attenuated. Furthermore, we demonstrated the interaction between the kinin B2 receptor and the TRPA1 channel in cisplatin-induced peripheral neuropathy since phospholipase C (PLC) and protein kinase C epsilon (PKCε) inhibitors attenuated the increase in mechanical and cold allodynia evoked by bradykinin and AITC in cisplatin-treated mice. Therefore, regulating the activation of signalling pathways downstream from the kinin B2 receptors activation and TRPA1 channel sensitisation can mitigate the painful peripheral neuropathy decurrent of the oncology treatment with cisplatin. Full article
(This article belongs to the Special Issue Potential Therapeutic Targets for the Treatment of Pathological Pain)
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Review

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13 pages, 246 KiB  
Review
Glial Modulator Antibiotics for Neuropathic Pain: Current Insights and Future Directions
by Alex J. Zimmerman, Nicholas Mangano, Grace Park, Amit K. Kaushal and Sergio D. Bergese
Pharmaceuticals 2025, 18(3), 346; https://doi.org/10.3390/ph18030346 - 28 Feb 2025
Viewed by 623
Abstract
Pathological pain is defined as pain that outlives its usefulness as a protective warning system and becomes debilitating, disrupting normal life function. Understanding the mechanism of transition from physiological to pathological pain is essential to provide the effective prevention of chronic pain. The [...] Read more.
Pathological pain is defined as pain that outlives its usefulness as a protective warning system and becomes debilitating, disrupting normal life function. Understanding the mechanism of transition from physiological to pathological pain is essential to provide the effective prevention of chronic pain. The main subcategories of pathological pain are nociceptive pain, neuropathic pain, and nociplastic pain. Glial cells play pivotal roles in the development and maintenance of each of these pathological pain states, specifically neuropathic pain. Consequently, targeting these cells has emerged as a promising therapeutic strategy, as limited efficacy and harmful adverse effects are associated with current pharmacotherapies. This paper aims to review specific antibiotics that modulate glial cells, which can be used to treat neuropathic pain. These antibiotics include minocycline, doxycycline, ceftriaxone, and azithromycin. The potential of these antibiotics appears promising, particularly given the extensive prior research and use of these antibiotics in humans for other illnesses. However, each presents its own set of limitations, ultimately making the translation from preclinical findings to human therapies for neuropathic pain challenging. Full article
(This article belongs to the Special Issue Potential Therapeutic Targets for the Treatment of Pathological Pain)
17 pages, 1148 KiB  
Review
The Importance of Visceral Hypersensitivity in Irritable Bowel Syndrome—Plant Metabolites in IBS Treatment
by Ewa Dudzińska, Andreas M. Grabrucker, Paweł Kwiatkowski, Robert Sitarz and Monika Sienkiewicz
Pharmaceuticals 2023, 16(10), 1405; https://doi.org/10.3390/ph16101405 - 3 Oct 2023
Cited by 7 | Viewed by 9778
Abstract
The visceral stimuli from the digestive tract are transmitted via afferent nerves through the spinal cord to the brain, where they are felt as pain. The overreaction observed in the brain of irritable bowel syndrome (IBS) patients may be due to increased peripheral [...] Read more.
The visceral stimuli from the digestive tract are transmitted via afferent nerves through the spinal cord to the brain, where they are felt as pain. The overreaction observed in the brain of irritable bowel syndrome (IBS) patients may be due to increased peripheral sensitivity to stimuli from the gastrointestinal tract. Although the exact pathway is uncertain, attenuation of visceral hypersensitivity is still of interest in treating IBS. It has been shown that stress stimulates the sympathetic nervous system while inhibiting the vagus nerve (VN). In addition, stress factors lead to dysbiosis and chronic low-grade inflammation of the intestinal mucosa, which can lead to lower gastrointestinal visceral hypersensitivity. Therefore, an important goal in the treatment of IBS is the normalization of the intestinal microflora. An interesting option seems to be nutraceuticals, including Terminalia chebula, which has antibacterial and antimicrobial activity against various pathogenic Gram-positive and Gram-negative bacteria. Additionally, short-term transcutaneous vagus nerve stimulation can reduce the stress-induced increase in intestinal permeability, thereby reducing inflammation. The conducted studies also indicate a relationship between the stimulation of the vagus nerve (VN) and the activation of neuromodulatory networks in the central nervous system. Therefore, it seems reasonable to conclude that a two-way action through stimulating the VN and using nutraceuticals may become an effective therapy in treating IBS. Full article
(This article belongs to the Special Issue Potential Therapeutic Targets for the Treatment of Pathological Pain)
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