, and metabolic energy balance ( Chatterjee et al . 2014 ). Although the underlying mechanism is not fully understood, adipose tissue inflammation has been acknowledged as a critical link between obesity and insulin resistance and type 2 diabetes, and
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Xiao-Bing Cui, Jun-Na Luan, Jianping Ye, and Shi-You Chen
S F Ahmed and C Farquharson
chronic inflammation which is often associated with altered systemic and local cytokine milieu. The mechanisms by which these inflammatory cytokines modulate linear growth and skeletal development are poorly understood, but an involvement of members of the
Sheng-Gao Tang, Xiao-Yu Liu, Ji-Ming Ye, Ting-Ting Hu, Ying-Ying Yang, Ting Han, and Wen Tan
( Maritim et al . 2003 ). Increased ROS exacerbate cardiac inflammation and fibrotic remodeling ( Rajesh et al . 2009 , Huynh et al . 2013 ). Additionally, hyperglycemia-induced glycation of proteins, lipids and nucleic acids can generate advanced
Yun Wang, Yue Zheng, Patsy M Nishina, and Jürgen K Naggert
inflammation, and obesity-associated cardiomyopathy. Obesity-induced inflammation is characterized in part by the infiltration of macrophages and other immune cells into white adipose tissue, and has been observed in both rodents and humans ( Wellen
Haiming Cao
development of metabolic disease ( Trujillo & Scherer 2006 ). Figure 1 Adipocytokines and metabolic inflammation in adipose tissue. Adipocytokines derived from adipose tissue are the results of intertwined interaction between adipocytes and immune cells that
Anna Cinkajzlová, Miloš Mráz, and Martin Haluzík
( Samsell et al. 2014 ). One of the main mechanisms responsible for the transition from simple obesity to subsequent cardiometabolic complications is the development of, at first, local and then systemic low-grade inflammation characterized by accumulation
Xi Tao, Yaxin Xu, Joseph Adu-Amankwaah, Zheng Gong, Yuxuan Wang, Fei Huang, and Hong Sun
result in myocardial inflammation and lipid accumulation, thus targeting the latter may be relevant in the prevention and treatment of stress-induced myocardial injury ( Scally et al. 2019 , Adu-Amankwaah et al. 2021 , Fiserova et al. 2022 ). As
Daniella B R Insuela, Julio B Daleprane, Luciana P Coelho, Adriana R Silva, Patrícia M R e Silva, Marco A Martins, and Vinicius F Carvalho
readings were recorded for 5 min following each nebulization. Penh averages were obtained at 1, 3 and 6 h after intranasal treatment with glucagon (1 μg/kg) or 0.9% NaCl sterile solution. LPS-induced lung inflammation Male A/J mice were anesthetized with
Jie Miao, Yacir Benomar, Sarah Al Rifai, Ghislaine Poizat, Laure Riffault, Delphine Crépin, and Mohammed Taouis
and humans and macrophages in humans ( Savage et al . 2001 , Patel et al . 2003 ), promoting inflammation and insulin resistance ( Savage et al . 2001 , Mojiminiyi & Abdella 2007 ). Furthermore, plasma resistin levels are increased in obese insulin
Eddy Himpe, Céline Degaillier, Astrid Coppens, and Ron Kooijman
of inflammation by chemoattractants such as interleukin-8 (IL8). This inflammatory cytokine is produced by monocytes and macrophages, and is also one of the most abundant cytokines produced by neutrophils, which triggers degranulation and oxidative
