Exploiting Injury-Induced Peripheral Opioid Receptor Changes in Novel Analgesic Development for Chronic Pain.

Front Pain Res (Lausanne)

Caventure Drug Discovery, Bloomfield Hills, MI, United States.

Published: April 2022

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9090307PMC
http://dx.doi.org/10.3389/fpain.2022.883164DOI Listing

Publication Analysis

Top Keywords

exploiting injury-induced
4
injury-induced peripheral
4
peripheral opioid
4
opioid receptor
4
receptor changes
4
changes novel
4
novel analgesic
4
analgesic development
4
development chronic
4
chronic pain
4

Similar Publications

Autophagy-targeting modulation to promote peripheral nerve regeneration.

Neural Regen Res

July 2025

Key Laboratory of Birth Defects and Women and Children's Diseases, Ministry of Education, Sichuan University, Chengdu, Sichuan Province, China.

Nerve regeneration following traumatic peripheral nerve injuries and neuropathies is a complex process modulated by diverse factors and intricate molecular mechanisms. Past studies have focused on factors that stimulate axonal outgrowth and myelin regeneration. However, recent studies have highlighted the pivotal role of autophagy in peripheral nerve regeneration, particularly in the context of traumatic injuries.

View Article and Find Full Text PDF

DNA-binding protein-A: a multitool in tubular epithelial cells.

Kidney Int

August 2024

Institute for Pathology, RWTH Aachen University Hospital, Aachen, Germany. Electronic address:

Acute kidney injury is still associated with high morbidity and mortality. Reichardt et al. investigated DNA-binding protein-A (Ybx3) in acute kidney injury induced by ischemia-reperfusion injury and found that mice lacking Ybx3 have altered mitochondrial function and increased antioxidant activity, making them more resistant to ischemia-reperfusion injury-acute kidney injury.

View Article and Find Full Text PDF

Short-term exposure to antimony induces hepatotoxicity and metabolic remodeling in rats.

Ecotoxicol Environ Saf

May 2023

China CDC Key Laboratory of Environment and Population Health, National Institute of Environmental Health, Chinese Center for Disease Control and Prevention, Beijing 100021, China; Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing 211166, China. Electronic address:

Antimony (Sb) poses a significant threat to human health due to sharp increases in its exploitation and application globally, but few studies have explored the pathophysiological mechanisms of acute hepatotoxicity induced by Sb exposure. We established an in vivo model to comprehensively explore the endogenous mechanisms underlying liver injury induced by short-term Sb exposure. Adult female and male Sprague-Dawley rats were orally administrated various concentrations of potassium antimony tartrate for 28 days.

View Article and Find Full Text PDF

Traumatic brain injury is one of the main causes of mortality and disability worldwide. Traumatic brain injury is characterized by a primary injury directly induced by the impact, which progresses into a secondary injury that leads to cellular and metabolic damages, starting in the first few hours and days after primary mechanical injury. To date, traumatic brain injury is not targetable by therapies aimed at preventing and/or limiting the outcomes of secondary damage but only by palliative therapies.

View Article and Find Full Text PDF

Eating your own fat to stay fit: lipophagy sustains lymphangiogenesis.

Autophagy

April 2023

Cell Death Research and Therapy Group, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium.

Lymphatic endothelial cells (LECs) exploit fatty acid oxidation (FAO) to grow and to maintain lymphatic vessel identity through the epigenetic regulation of the essential transcription factor PROX1. In our recent study, we found that LEC-specific loss of prevents injury-induced lymphangiogenesis . Inadequate degradation of lipid droplets (LDs) caused by genetic ablation of in LECs disturbs mitochondrial fitness, and reduces mitochondrial FAO and acetyl-CoA levels, ultimately affecting PROX1-mediated epigenetic regulation of CPT1A and key lymphatic markers, most importantly FLT4/VEGFR3.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!