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EDITORIAL article

Front. Pharmacol., 17 October 2023
Sec. Inflammation Pharmacology
This article is part of the Research Topic Global Excellence in Inflammation Pharmacology View all 5 articles

Editorial: Global excellence in inflammation pharmacology

  • 1Neurobiology Laboratory, Department of Health and Human Services, National Institute of Environmental Health Sciences, National Institutes of Health, Durham, NC, United States
  • 2Division of Hematology and Blood Research Center, Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States

Editorial on the Research Topic
Global excellence in inflammation pharmacology

In our day-to-day life, acute inflammation occurs commonly as a part of the body’s regular healing process post an injury or infection and is usually short term in nature. The problem arises when this inflammation becomes chronic, due to the failure in resolving itself, leading to a spectrum of diseases which explicitly contributes to more than 50% of worldwide mortality (GBD, 2017 Causes of Death Collaborators, 2018; Furman et al., 2019) Thus, prolonged inflammation is emerging as a serious threat to the global population and socioeconomic sustainability. Advancements in effective anti-inflammatory therapies have been significantly evolving, but challenges persist (Netea et al., 2017). Hence, scientists globally or in global alliance, with varied scientific perspectives, are actively working on finding out pharmacological interventions against inflammation associated pathogenesis and diseases. A major part of the research is also focused on scientific advancements of evolving therapeutic strategies by identifying the central signaling molecules or cascades involved in the onset and progression of chronic inflammation. This special edition Research Topic Global Excellence in Inflammation Pharmacology aims in emphasizing on the recent progress made in these fields, highlighting the diversified research performed across the entire breadth of Inflammation Pharmacology and providing insights to it. This Research Topic comprises of four extensive literature reviews discussing the potential pharmacological interventions and their allied risk in inflammation associated diseases.

One of the prevalent inflammatory diseases with approximately 500 million people suffering worldwide, is osteoarthritis (OA). OA involves joint inflammation and is degenerative in nature (Hunter et al., 2020). Literature suggests that peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), the mitochondrial biogenesis master regulator, is downregulated in OA by molecules like AGE. The review article by Wang et al. discusses the chondroprotective role of PGC-1α in OA and provides an understanding of its mechanistic regulation by pathways like AMPK/SIRT1, SIRT3, mTOR, etc., in delaying OA onset and progression. They elaborate how PGC-1α inhibits apoptosis and alters mitochondrial biogenesis, providing protection to the chondrocytes. They also discuss reports on PGC-1α modulating natural compounds, chemical drugs and novel nanohybrid formulations for the treatment of OA. This review sheds light on the up-to-date developments of therapeutic strategies for OA along with providing a detailed understanding on the pathogenesis of OA.

Another article by Huang et al. reviews the therapeutic potential of natural bioactive compound Chlorogenic acid and how it acts as a protective molecule against inflammation driven conditions such as cardio-cerebrovascular pathology and diabetes mellitus. It exerts anti-inflammatory potential by the inhibition of pro-inflammatory cytokines, prostaglandin E2 and nitric oxide along with modulation of key cellular signaling pathways like NF-κB, MAPK and Nrf2. They further discuss the limitation of the use of chlorogenic acid due to its inherent low bioavailability and how this is overcome by upgraded delivery systems, positively regulating the release mechanisms, stability, and bioactivity of Chlorogenic acid, making it a more promising pharmacologically active anti-inflammatory intervention.

“Metabolic syndrome,” a relatively newly recognized pathology, primarily comprises of different detrimental inflammatory conditions of the body that leads to hypertension, hyperglycemia, insulin resistance, obesity, hypercholesterolemia, and so on. This is intricately associated with global health risk, precisely increasing development of cardiovascular and atherosclerotic diseases. In their thorough review article, Collotta et al. discuss in detail about the current advancements of Janus Kinase (JAK) inhibitors for their efficacy in treating metabolic syndrome, highlighting the importance of JAK-STAT signaling pathways in such chronic inflammatory conditions.

Continuing with the discussion of the JAK inhibitors in inflammatory diseases, in their systemic review, Xu et al. extensively discuss about the meta-analysis on the efficacy of JAK inhibitors in immune-mediated inflammatory diseases (IMID) and the side effects reported such as higher risk of herpes zoster infection in patients associated with the use of JAK inhibitors. Herpes zoster (or shingles) is a viral infection caused by the reactivation of the varicella-zoster virus in patients who have a history of chickenpox infection. Their study indicates that except for a few JAK inhibitors, like peficitinib, baricitinib, and tofacitinib, there is no association of higher risk of herpes zoster infection in patients with IMIDs.

Author contributions

SS: Conceptualization, Writing–original draft, Writing–review and editing. SG: Writing–original draft.

Funding

The authors declare that no financial support was received for the research, authorship, and/or publication of this article.

Conflict of interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Publisher’s note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

References

Furman, D., Campisi, J., Verdin, E., Carrera-Bastos, P., Targ, S., Franceschi, C., et al. (2019). Chronic inflammation in the etiology of disease across the life span. Nat. Med. 25 (12), 1822–1832. doi:10.1038/s41591-019-0675-0

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GBD 2017 Causes of Death Collaborators (2018). Global, regional, and national age-sex-specific mortality for 282 causes of death in 195 countries and territories, 1980-2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet 392 (10159), 1736–1788. doi:10.1016/S0140-6736(18)32203-7

PubMed Abstract | CrossRef Full Text | Google Scholar

Hunter, D. J., March, L., and Chew, M. (2020). Osteoarthritis in 2020 and beyond: a lancet commission. Lancet 396 (10264), 1711–1712. doi:10.1016/S0140-6736(20)32230-3

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Netea, M. G., Balkwill, F., Chonchol, M., Cominelli, F., Donath, M. Y., Giamarellos-Bourboulis, E. J., et al. (2017). A guiding map for inflammation. Nat. Immunol. 18 (8), 826–831. doi:10.1038/ni.3790

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Keywords: inflammation, pharmacological interventions, global alliance, therapeutics, diseases

Citation: Saha S and Ghosh S (2023) Editorial: Global excellence in inflammation pharmacology. Front. Pharmacol. 14:1307503. doi: 10.3389/fphar.2023.1307503

Received: 04 October 2023; Accepted: 10 October 2023;
Published: 17 October 2023.

Edited and reviewed by:

Paola Patrignani, University of Studies G d'Annunzio Chieti and Pescara, Italy

Copyright © 2023 Saha and Ghosh. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Sukanya Saha, sukanya.saha@nih.gov 

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.