THE INSIDER - FALL 2024

Dr. Sohel Quazi, Assistant Professor of Biology, recently published an article titled "TLR4 Induced TRPM2 Mediated Neuropathic Pain," in the peer-reviewed journal Frontiers in Pharmacology. Through collaboration with The University of Texas at Tyler’s Fisch College of Pharmacy, the research team has successfully identified a new mechanism for pain pathway. In essence, the research from Dr. Quazi and his colleagues explores how neuropathic pain is linked to transient receptor potential channel Melastatin 2 (TRPM2), a calcium channel activated by Toll-like receptor 4 (TLR4). It delves into the mechanisms of pain development, emphasizing how TRPM2 modulates oxidative stress and inflammation in neurons, contributing to persistent pain. The study suggests that targeting TRPM2 may present new therapeutic opportunities for managing neuropathic pain.

MECHANISM OF TLR4 INDUCED TRPM2 MEDIATED NEUROPATHIC PAIN, DESIGNED BY DR. QUAZI

Summarily, the new mechanism for pain pathway is important because it addresses the question of how to stop neuropathic pain by blocking the pathway and, in turn, stopping pain. While the role of TRPM2 ion channels and their association with Toll-like receptors in pain management needs to be studied in more detail for the development of effective strategies to treat neuropathic pain, a next step could be the development of a drug. Dr. Quazi's full published article can be accessed by visiting the Frontiers in Pharmacology website (www.frontiersin.org).

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