To reveal the trajectories of smooth muscle cell (SMC) transdifferentiation during atherosclerosis and to identify molecular targets for disease therapy, researchers combined SMC fate mapping and single-cell RNA sequencing of both mouse and human atherosclerotic plaques.
Pan Huize, Xue Chenyi, Auerbach Benjamin J., Fan Jiaxin, Bashore Alexander C., Cui Jian, Yang Dina Y., Trignano Sarah B., Liu Wen, Shi Jianting, Ihuegbu Chinyere O., Bush Erin C., Worley Jeremy, Vlahos Lukas, Laise Pasquale, Solomon Robert A., Connolly Edward S., Califano Andrea, Sims Peter A., … Reilly Muredach P. (n.d.). Single-Cell Genomics Reveals a Novel Cell State During Smooth Muscle Cell Phenotypic Switching and Potential Therapeutic Targets for Atherosclerosis in Mouse and Human. Circulation, 0(0). https://doi.org/10.1161/CIRCULATIONAHA.120.048378Cite
The authors provide a comprehensive perspective on the pivotal role of NLR-family pyrin domain-containing protein 3 (NLRP3) inflammasome activation in aggravating oxidative stress and endothelial dysfunction and the possible underlying mechanisms.
The authors provide an overview of the available knowledge of body wasting and physical frailty in patients with cardiovascular illness, particularly focusing on patients with heart failure in whom most of the available data has been gathered.
Bielecka‐Dabrowa, A., Ebner, N., Santos, M. R. dos, Ishida, J., Hasenfuss, G., & Haehling, S. von. (n.d.). Cachexia, muscle wasting, and frailty in cardiovascular disease. European Journal of Heart Failure, n/a(n/a). https://doi.org/10.1002/ejhf.2011Cite
Non-enzymatic chitinase-3 like-protein-1 (CHI3L1) binds to chitin, heparin, and hyaluronic acid, and is regulated by ECM changes, cytokines, growth factors, drugs, and stress. This review summarizes the potential roles and mechanisms of CHI3L1 in oncogenesis and disease pathogenesis, then posits investigational strategies for targeted therapies.
Overexpression of ANRIL transcript NR_003529 increased monocyte adhesion to endothelial cells (ECs) and transendothelial monocyte migration (TEM), whereas knockdown of NR_003529 expression reduced monocyte adhesion to ECs and TEM.