Decoding the Biology of Pain for Precision Therapies
Pain is more than a symptom; it is a complex, debilitating global health challenge with profound personal and societal costs. At the PROPA Lab, we are dedicated to dissecting pain at its most fundamental level. We move beyond traditional approaches to unravel the intricate molecular and genetic dialogues that initiate and sustain pain, aiming to rewrite the future of pain management. Our research in pain biology focuses on the molecular, genetic, and epigenetic mechanisms underlying neuropathic and chronic pain, with particular emphasis on trigeminal and neuropathic pain models. Using transcriptomic, molecular, and behavioral approaches, we investigate how gene regulation, non-coding RNAs, and transcriptional control in sensory neurons and pain-processing nuclei contribute to nociceptive hypersensitivity, anxiety-like behaviors, and the transition from acute to chronic pain. Our studies have identified key regulators such as Y-box binding protein 3 (YBX3) and circadian genes (e.g., PER1) as critical drivers of mechanical allodynia and pain-related affective changes in trigeminal neuralgia models.
In parallel, we explore neuroinflammation, oxidative stress, and epigenetic regulation as central mechanisms sustaining chronic pain. Our work demonstrates that TET1-mediated epigenetic control of TNF-α, dysregulated lncRNA and mRNA networks, and mitochondrial dysfunction play pivotal roles in neuropathic pain and temporomandibular joint pain.
We further investigate nanozyme-based and small-molecule interventions that target oxidative stress, inflammatory signaling (TNF-α/NF-κB), and neuroimmune pathways to alleviate pain in preclinical models. Together, these studies provide mechanistic insights and support the development of mechanism-driven, translational pain therapies .
Key Research Terms
- The Chronic Pain Enigma: Why does acute pain sometimes transition into a persistent, chronic condition? We are investigating the molecular “switch”—the drivers and signaling cascades—responsible for this transition. By understanding the mechanisms behind pain chronification, we aim to develop interventions that can halt or reverse this process.
- Nanozyme-Based Neuromodulation: We are pioneering the use of nanozymes—nanoparticles with enzyme-like activity—as a novel class of therapeutics for neuropathic pain. Our strategies are multi-faceted, designing nanozymes that can simultaneously tackle oxidative stress, promote mitochondrial repair, and modulate neuroimmune interactions. This multi-target approach represents a new frontier in targeted, effective, and non-addictive pain relief.