In this Issue
Clinical Science (31 July 2019) 133 (14): 1549–1565.
New therapeutic targets for the prevention of infectious acute exacerbations of COPD: role of epithelial adhesion molecules and inflammatory pathways
Brianna Atto; Mathew Suji Eapen; Pawan Sharma; Urs Frey; Alaina J. Ammit; James Markos; Collin Chia; Josie Larby; Greg Haug; Heinrich C. Weber; George Mabeza; Stephen Tristram; Stephen Myers; Dominic P. Geraghty; Katie L. Flanagan; Philip M. Hansbro; Sukhwinder Singh Sohal
Clinical Science (31 July 2019) 133 (14): 1663–1703.
Clinical Science (31 July 2019) 133 (14): 1581–1585.
Clinical Science (31 July 2019) 133 (14): 1603–1607.
Soluble ST2 promotes oxidative stress and inflammation in cardiac fibroblasts: an in vitro and in vivo study in aortic stenosis
Lara Matilla; Jaime Ibarrola; Vanessa Arrieta; Amaia Garcia-Peña; Ernesto Martinez-Martinez; Rafael Sádaba; Virginia Alvarez; Adela Navarro; Amaya Fernández-Celis; Alicia Gainza; Enrique Santamaría; Joaquín Fernández-Irigoyen; Antoni Bayes-Genis; Patrick Rossignol; Natalia López-Andrés
Clinical Science (31 July 2019) 133 (14): 1537–1548.
Down-regulation of lncRNA XIST inhibits cell proliferation via regulating miR-744/RING1 axis in non-small cell lung cancer
Clinical Science (31 July 2019) 133 (14): 1567–1579.
Jean-François Thibodeau; Jean-Christophe Simard; Chet E. Holterman; Amélie Blais; Marie-Pier Cloutier; Thalia Medeiros; Martin Leduc; Brigitte Grouix; François A. Leblond; Dylan Burger; Richard L. Hébert; Christopher R.J. Kennedy; Lyne Gagnon
Clinical Science (31 July 2019) 133 (14): 1587–1602.
RIPK1 inhibitor Cpd-71 attenuates renal dysfunction in cisplatin-treated mice via attenuating necroptosis, inflammation and oxidative stress
Jia-nan Wang; Ming-ming Liu; Fang Wang; Biao Wei; Qin Yang; Yu-ting Cai; Xin Chen; Xue-qi Liu; Ling Jiang; Chao Li; Xiao-wei Hu; Ju-tao Yu; Tao-tao Ma; Juan Jin; Yong-gui Wu; Jun Li; Xiao-ming Meng
Clinical Science (31 July 2019) 133 (14): 1609–1627.
Cover ImageIn the latest issue of Clinical Science (volume 133, issue 14), Sokeechand and Trigatti provide a commentary on the junction adhesion molecule-like (JAM-L) protein's potential as a therapeutic target for atherosclerosis. This cover shows some of the key steps in the initiation and progression of atherosclerotic plaques that appear to be influenced by JAM-L. These include monocyte and neutrophil recruitment, and oxidised LDL-stimulated cytokine production by macrophages.