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Obesity has reached epidemic proportions in the Western society and is increasing in the developing world. It is considered as one of the major contributors to the global burden of disability and chronic diseases, including autoimmune, inflammatory and degenerative diseases. Research conducted on obesity and its complications over the last two decades has transformed the outdated concept of white adipose tissue (WAT) merely serving as an energy depot. WAT is now recognized as an active and inflammatory organ capable of producing a wide variety of factors known as adipokines. These molecules participate through endocrine, paracrine, autocrine or juxtacrine crosstalk mechanisms in a great variety of physiological or pathophysiological processes, regulating food intake, insulin sensitivity, immunity and inflammation. Although initially restricted to metabolic activities (regulation of glucose and lipid metabolism), adipokines currently represent a new family of proteins that can be considered key players in the complex network of soluble mediators involved in the pathophysiology of immune/inflammatory diseases. However, the complexity of the adipokine network in the pathogenesis and progression of inflammatory diseases has posed, since the beginning, the important question of whether it may be possible to target the mechanism(s) by which adipokines contribute to disease selectively without suppressing their physiological functions. Here, we explore in depth the most recent findings concerning the involvement of adipokines in inflammation and immune responses, in particular in rheumatic, inflammatory and degenerative diseases. We also highlight several possible strategies for therapeutic development and propose that adipokines and their signalling pathways may represent innovative therapeutic strategies for inflammatory disorders.
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http://dx.doi.org/10.1111/bph.14181 | DOI Listing |
Mol Cell Neurosci
September 2025
Biomedical and Forensic Science, School of Human Sciences, University of Derby, Derby, DE22 1GB, United Kingdom; Life and Health Sciences, University of Roehampton, London, SW15 5PH, United Kingdom. Electronic address:
Emerging evidence indicates that apelin, an adipokine, plays a critical role in numerous biological functions and may hold potential for therapeutic applications; however, its efficacy is constrained by rapid plasma degradation. Thus, the search for novel apelin analogues with reduced susceptibility to plasma degradation is ongoing. We have previously shown novel modified apelin-13 analogues, providing exciting opportunities for potential therapeutic development against Alzheimer's disease.
View Article and Find Full Text PDFOsteoarthritis Cartilage
September 2025
Department of Inflammation and Ageing, School of Infection, Inflammation and Immunology, College of Medicine and Health, University of Birmingham, Birmingham B15 2TT, United Kingdom; National Institute for Health and Care Research (NIHR) Birmingham Biomedical Research Centre, UK. Electronic address:
Objective: To investigate the inflammatory profiles of adipose tissues from patients with osteoarthritis (OA), comparing the joint-associated adipose tissues, infrapatellar fat pad (IFP) and sub-synovial (SSAT)with subcutaneous adipose tissue (SCAT), and to explore adipose-joint cell crosstalk.
Design: RNA sequencing was performed on autologous IFP, SSAT, and SCAT from six patients. The adipose tissue secretome was profiled using targeted proteomics.
Int Immunopharmacol
September 2025
Department of Traditional Chinese Medicine, Shanghai Children's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. Electronic address:
Background: Leptin is a proinflammatory adipokine asthmatic biomarker and macrophage necroptosis are previously reported to be involved in asthmatic airway inflammation. However, whether leptin worsen airway inflammation via mediating macrophage necroptosis remains elusive. We investigated the role of the leptin on regulating macrophage necroptosis in the development of asthma.
View Article and Find Full Text PDFScience
September 2025
Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
Ventricular tachycardia disrupts the heart's coordinated pump function, leading to sudden cardiac death. Neutrophils, which are recruited in high numbers to the ischemic myocardium, promote these arrhythmias. Comparing neutrophils with macrophages, we found that resistin-like molecule γ ( or RELMγ) was the most differentially expressed gene in mouse infarcts.
View Article and Find Full Text PDFCurr Med Sci
September 2025
Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Adipokines, including C1q/tumor necrosis factor (TNF)-related proteins (CTRPs), adiponectin, TNF-α, and leptin, are crucial bioactive molecules that are secreted by adipose tissue and circulate in the bloodstream. To date, 15 members of the CTRP family, which are collectively classified as part of the C1q/TNF superfamily, have been identified. Among these, CTRP3 stands out as a unique adipokine because of its distinct structural and functional properties.
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