Nonalcoholic fatty liver disease (NAFLD) is a progressive liver disease with ever-growing incidence in the industrialized world. It starts with the simple accumulation of lipids in the hepatocyte and can progress to the more severe nonalcoholic steatohepatitis (NASH), which is associated with inflammation, fibrosis, and cirrhosis. There is increasing awareness that reactive oxygen species and electrophiles are implicated in the pathogenesis of NASH. Transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) is a positive regulator of the expression of a battery of genes involved in the protection against oxidative/electrophilic stress. In rodents, Nrf2 is also known to participate in hepatic fatty acid metabolism, as a negative regulator of genes that promote hepatosteatosis. We review relevant evidence in the literature that these two mechanisms may contribute to the protective role of Nrf2 in the development of hepatic steatosis and in the progression to steatohepatitis, particularly in young animals. We propose that age may be a key to explain contradictory findings in the literature. In summary, Nrf2 mediates the crosstalk between lipid metabolism and antioxidant defense mechanisms in experimental models of NAFLD, and the nutritional or pharmacological induction of Nrf2 represents a promising potential new strategy for its prevention and treatment.

Spinal cord injury (SCI) is a devastating event with a tremendous impact in the life of the affected individual and family. Traumatic injuries related to motor vehicle accidents, falls, sports, and violence are the most common causes. The majority of spinal lesions is incomplete and occurs at cervical levels of the cord, causing a disruption of several ascending and descending neuronal pathways. Additionally, many patients develop chronic pain and describe it as burning, stabbing, shooting, or shocking and often arising with no stimulus. Less frequently, people with SCI also experience pain out of context with the stimulus (e.g., light touch). While abolishment of the endogenous descending inhibitory circuits is a recognized cause for chronic pain, an increasing number of studies suggest that uncontrolled release of pro-and anti-inflammatory mediators by neurons, glial, and immune cells is also important in the emergence and maintenance of SCI-induced chronic pain. This constitutes the topic of the present mini-review, which will focus on the importance of neuro-immune dysregulation for pain after SCI.

Pain is a complex experience, encompassing physiological and psychological components. Amongst the different types of pain, neuropathic pain, resulting from injuries to the peripheral or central nervous system, still constitutes a challenge for researchers and clinicians. Nerve growth factor (NGF) is currently regarded as a key contributor and may serve as a therapeutic target in many types of pain, likely including neuropathic pain. Here, we reviewed the role of NGF in neuropathic pain of peripheral and central origin, also addressing its potential use as a pharmacological target to better help patients dealing with this condition that severely impacts the everyday life. For this, we conducted a search in the databases PubMed and Scopus. Our search resulted in 1103 articles (458 in PubMed and 645 in Scopus). Only articles related to the involvement of NGF in pain or articles that approached its potential use as a target in treatment of pain symptoms were included. Duplicates were eliminated and 274 articles were excluded. After careful analysis, 23 articles were selected for review. Original articles studying the role of NGF in pathology as well as its modulation as a possible therapeutic target were included. We found that NGF is widely regarded as a key player in neuropathic pain and seen as a putative therapeutic target. However, evidence obtained from years of clinical trials highlights the toxic adverse effects of anti-NGF therapeutics, precluding its use in clinical context. Further studies are, thus, needed to improve treatment of chronic neuropathic pain.