Cytokine & Growth Factor Reviews最新文献

Neurotrophic factors are a family of proteins that promote the growth and survival of both developing and mature neurons. Extensive preclinical studies have demonstrated neuroprotective properties conferred by ciliary neurotrophic factor (CNTF) in a variety of neuron types across several species. Neuroprotection that CNTF confers slows or prevents neuron loss and appears to be agnostic to the nature of the neurodegenerative mutation or injury. However, translation of these studies to the clinic remains a challenge due in part to delivery barriers inherent to the central nervous system and the short half-life of CNTF. The molecular effect of CNTF delivered by a variety of strategies in model systems has been extensively studied in the neural retina. Long-term retinal neuroprotection has been documented using encapsulated cells that have been genetically modified to produce a stable source of CNTF. Clinical trials have shown that CNTF is well tolerated for use in the human retina. This review focuses on the mechanism of action of CNTF and its potential as a therapeutic agent in retinal disease, with a focus on macular telangiectasia type 2 where CNTF has shown efficacy in slowing the rate of ellipsoid zone loss.

Pulmonary hypertension is one of the most intractable cardiovascular diseases in the world today. The current pharmacological treatments can temporarily relieve symptoms, but the therapeutic effect is unsatisfactory in advanced pulmonary hypertension with severe pulmonary vascular remodeling and right ventricular hypertrophy. The nuclear receptor superfamily is a vital class of transcriptional regulators in the human body. Extensive research has demonstrated that these regulators play pivotal roles in a multitude of physiological processes and are involved in the regulation of the pathogenesis of a variety of pathological diseases, providing potential therapeutic targets for pulmonary hypertension. The targeting of nuclear receptors, such as MR, PPARγ, and NUR77, has demonstrated potential in improving pulmonary vascular remodeling and preventing the progression of experimental pulmonary hypertension. However, further in-depth mechanistic exploration and large-scale preclinical studies are necessary to facilitate eventual clinical application. In this review, we describe in detail the various types of nuclear receptors that affect the function of pulmonary vascular endothelial cells and smooth muscle cells by regulating inflammation, oxidative stress, metabolism, and other processes, thereby affecting the prognosis of pulmonary hypertension, and highlight the clinical therapeutic potential of nuclear receptors. Intensive research on the regulatory role of nuclear receptors in pulmonary hypertension has yielded new avenues for targeted therapy of pulmonary hypertension and has prompted the exploration of new therapeutic strategies to combat this life-threatening disease.

Interleukin (IL)-1β is a pro-inflammatory cytokine largely produced by cells of the innate immune system in response to tissue damage or to the presence of pathogens. IL-1β-driven inflammation is an established contributor to many disease processes and thus there is great interest in understanding its regulation. This review focusses on the mechanisms involved in the secretion of IL-1β by macrophages. As IL-1β secretion does not follow the conventional ER-Golgi secretory pathway, various mechanisms for IL-1β secretion are proposed, with evidence suggesting that multiple pathways may exist. This review considers the proposed mechanisms determining the secretory pathway of IL-1β.

Oligodendrocytes (OLs) facilitate the myelination within the central nervous system (CNS). Neuronal axons are originally devoid of myelin and acquire myelination during development. OLs are derived from oligodendrocyte precursor cells (OPCs) during development, and this ability to differentiate persists throughout maturity. The abnormal differentiation of oligodendrocytes leads to various neurological disorders and neurodegenerative diseases characterized by disruptions in myelin formation, which is crucial for proper nerve function. In order to develop suitable strategies for their treatments an intimate knowledge of oligodendrocytes differentiation and maturation processes is a pre-requisite. Numerous unique growth factors like PDGF, IGF-1, FGF, etc. function at different phases of lineage specification. The activity of these factors, in turn, is influenced by synergy with other molecules, such as chemokines to control the proliferation of OL precursor cells. The role of growth factors in oligodendrogenesis needs to be revisited constantly with the regular inflow of studies on OL development. An understanding of how different growth factors influence oligodendrogenesis will facilitate their recruitment in stem cell therapy protocols, in vivo studies on OPC and OL development. The end goal of such studies is to enhance neuroregeneration in various demyelinating pathological illnesses. We provide an overview of the research carried out on the role of growth factors on differentiation and maturation of oligodendrocytes. Besides, efforts have been made to identify areas requiring further investigation.

Ferroptosis, an iron-dependent cell death driven by lipid peroxidation, has emerged as a pivotal mechanism in cancer biology with significant therapeutic potential. Immune cells, both innate and adaptive, are integral in detecting and eliminating tumor cells, yet their response is intricately modulated by ferroptosis. While cancer cell ferroptosis stimulates anti-tumor immunity, ferroptosis in immune cells undermines their effectiveness, compromising overall immune surveillance. The intricate crosstalk between ferroptosis and immune responses is pivotal in tumor progression and therapeutic outcomes, shaping both cancer resistance and treatment effectiveness. This review explores the multifaceted relationship between ferroptosis and immune function in cancer, offering insights into how these processes intersect to shape tumor immunity and guide immunotherapy strategies. We highlight cutting-edge research, uncover key molecular mechanisms, and outline promising avenues for future studies and therapeutic interventions in this evolving field.

Systemic lupus erythematosus (SLE) is a chronic, multisystemic, heterogenic and complex autoimmune disease. Similarly, obesity is a chronic condition characterized by excessive adipose tissue and a sustained state of inflammation. Both conditions have shown increasing incidence in recent years, with evidence of closely intertwined pathogenesis. Leptin, a peptide hormone derived from adipokines and produced in white adipose tissue, exhibits functions like those of pro-inflammatory cytokines and plays a key role in regulating the immune system. There is a clear connection linking obesity and SLE. Extensive studies indicate that obese patients have a higher susceptibility to developing immunological diseases, such as SLE, often at younger ages and with an elevated risk of complications. Leptin appears to play a significant role in immune responses and has been implicated as a mediator in the pathogenesis of SLE and obesity. This hormone contributes to chronic inflammation and immune dysfunction. Elevated leptin levels have been identified in patients with SLE and have been associated with increased disease risk, higher disease activity, and a greater likelihood of complications. Similarly, increased leptin levels have been observed in individuals with obesity and metabolic syndrome. This evidence suggests that leptin may serve as a biomarker and a potential therapeutic target for managing SLE, particularly in obese patients.