Filippo Crea
doi : 10.1093/eurheartj/ehab747
European Heart Journal, Volume 42, Issue 42, 7 November 2021, Pages 4285–4289
Mark Nicholls
doi : 10.1093/eurheartj/ehab199
European Heart Journal, Volume 42, Issue 42, 7 November 2021, Pages 4290–4297
Mark Nicholls
doi : 10.1093/eurheartj/ehab244
European Heart Journal, Volume 42, Issue 42, 7 November 2021, Pages 4292–4294
Yoav Michowitz, Mads Brix Kronborg, Michael Glikson, Jens Cosedis Nielsen
doi : 10.1093/eurheartj/ehab699
European Heart Journal, Volume 42, Issue 42, 7 November 2021, Page 4295
Giovanna Liuzzo, Massimo Volpe
doi : 10.1093/eurheartj/ehab616
European Heart Journal, Volume 42, Issue 42, 7 November 2021, Pages 4296–4297
Xin Jiang, Yong-Jian Zhu, Yu-Ping Zhou, Fu-Hua Peng, Lan Wang, Wei Ma, Yun-Shan Cao, Xin Pan, Gang-Cheng Zhang, Feng Zhang, Fen-Ling Fan, Bing-Xiang Wu, Wei Huang, Zhen-Wen Yang, Cheng Hong, Meng-Tao Li, Yi-Ning Wang, Xi-Qi Xu, Duo-Lao Wang, Shu-Yang Zhang, Zhi-Cheng Jing
doi : 10.1093/eurheartj/ehab599
European Heart Journal, Volume 42, Issue 42, 7 November 2021, Pages 4298–4305
This study aimed to assess the clinical characteristics and long-term survival outcome in patients with Takayasu’s arteritis-associated pulmonary hypertension (TA-PH).
Yoshihiro Fukumoto
doi : 10.1093/eurheartj/ehab688
European Heart Journal, Volume 42, Issue 42, 7 November 2021, Pages 4306–4308
Lotte C A Stiekema, Lisa Willemsen, Yannick Kaiser, Koen H M Prange, Nicholas J Wareham, S Matthijs Boekholdt, Carlijn Kuijk, Menno P J de Winther, Carlijn Voermans, Matthias Nahrendorf, Erik S G Stroes, Jeffrey Kroon
doi : 10.1093/eurheartj/ehab465
European Heart Journal, Volume 42, Issue 42, 7 November 2021, Pages 4309–4320
Preclinical work indicates that low-density lipoprotein cholesterol (LDL-C) not only drives atherosclerosis by directing the innate immune response at plaque level but also augments proinflammatory monocyte production in the bone marrow (BM) compartment. In this study, we aim to unravel the impact of LDL-C on monocyte production in the BM compartment in human subjects.
Laurent Yvan-Charvet, Marit Westerterp
doi : 10.1093/eurheartj/ehab630
European Heart Journal, Volume 42, Issue 42, 7 November 2021, Pages 4321–4323
Renato Quispe, Seth Shay Martin, Erin Donelly Michos, Isha Lamba, Roger Scott Blumenthal, Anum Saeed, Joao Lima, Rishi Puri, Sarah Nomura, Michael Tsai, John Wilkins, Christie Mitchell Ballantyne, Stephen Nicholls, Steven Richard Jones, Mohamed Badreldin Elshazly
doi : 10.1093/eurheartj/ehab432
European Heart Journal, Volume 42, Issue 42, 7 November 2021, Pages 4324–4332
Emerging evidence suggests that remnant cholesterol (RC) promotes atherosclerotic cardiovascular disease (ASCVD). We aimed to estimate RC-related risk beyond low-density lipoprotein cholesterol (LDL-C) and apolipoprotein B (apoB) in patients without known ASCVD.
Jan Borén, Chris J Packard
doi : 10.1093/eurheartj/ehab531
European Heart Journal, Volume 42, Issue 42, 7 November 2021, Pages 4333–4335
Phuong Tran Pham, Daiju Fukuda, Sachiko Nishimoto, Joo-Ri Kim-Kaneyama, Xiao-Feng Lei, Yutaka Takahashi, Tomohito Sato, Kimie Tanaka, Kumiko Suto, Yutaka Kawabata, Koji Yamaguchi, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Kenji Shimada, Yasuhisa Kanematsu, Yasushi Takagi, Michio Shimabukuro, Mitsutoshi Setou, Glen N Barber, Masataka Sata
doi : 10.1093/eurheartj/ehab249
European Heart Journal, Volume 42, Issue 42, 7 November 2021, Pages 4336–4348
Lifestyle-related diseases promote atherosclerosis, a chronic inflammatory disease; however, the molecular mechanism remains largely unknown. Endogenous DNA fragments released under over-nutrient condition provoke sterile inflammation through the recognition by DNA sensors. Here, we investigated the role of stimulator of interferon genes (STING), a cytosolic DNA sensor, in atherogenesis.
Donato Santovito, Sabine Steffens
doi : 10.1093/eurheartj/ehab300
European Heart Journal, Volume 42, Issue 42, 7 November 2021, Pages 4349–4351
Anahita Mojiri, Brandon K Walther, Chongming Jiang, Gianfranco Matrone, Rhonda Holgate, Qiu Xu, Elisa Morales, Guangyu Wang, Jianhua Gu, Rongfu Wang, John P Cooke
doi : 10.1093/eurheartj/ehab547
European Heart Journal, Volume 42, Issue 42, 7 November 2021, Pages 4352–4369
Hutchinson-Gilford progeria syndrome (HGPS) is an accelerated ageing syndrome associated with premature vascular disease and death due to heart attack and stroke. In HGPS a mutation in lamin A (progerin) alters nuclear morphology and gene expression. Current therapy increases the lifespan of these children only modestly. Thus, greater understanding of the underlying mechanisms of HGPS is required to improve therapy. Endothelial cells (ECs) differentiated from induced pluripotent stem cells (iPSCs) derived from these patients exhibit hallmarks of senescence including replication arrest, increased expression of inflammatory markers, DNA damage, and telomere erosion. We hypothesized that correction of shortened telomeres may reverse these measures of vascular ageing.
Rosalinda Madonna
doi : 10.1093/eurheartj/ehab587
European Heart Journal, Volume 42, Issue 42, 7 November 2021, Pages 4370–4372
Hongtu Cui, Yanghui Chen, Ke Li, Rui Zhan, Mingming Zhao, Yangkai Xu, Zhiyong Lin, Yi Fu, Qihua He, Paul C Tang, Ienglam Lei, Jifeng Zhang, Chenze Li, Yang Sun, Xinhua Zhang, Tiffany Horng, Hong S Lu, Y Eugene Chen, Alan Daugherty, Daowen Wang, Lemin Zheng
doi : 10.1093/eurheartj/ehab605
European Heart Journal, Volume 42, Issue 42, 7 November 2021, Pages 4373–4385
Aortic aneurysm and dissection (AAD) are high-risk cardiovascular diseases with no effective cure. Macrophages play an important role in the development of AAD. As succinate triggers inflammatory changes in macrophages, we investigated the significance of succinate in the pathogenesis of AAD and its clinical relevance.
Rohan Bhandari, Scott J Cameron
doi : 10.1093/eurheartj/ehab514
European Heart Journal, Volume 42, Issue 42, 7 November 2021, Pages 4386–4388
Chiara Baldini, Francesca Romana Moriconi, Sara Galimberti, Peter Libby, Raffaele De Caterina
doi : 10.1093/eurheartj/ehab447
European Heart Journal, Volume 42, Issue 42, 7 November 2021, Pages 4389–4400
Inflammation contributes centrally to cardiovascular diseases, and anti-inflammatory treatments can reduce cardiovascular events. The JAK–STAT pathway is an emerging target in inflammation, mainly in rheumatoid arthritis (RA) and chronic myeloproliferative neoplasms (MPNs), disorders that heighten cardiovascular risk. The aim of this study was to review the international literature on the relationship between dysregulation of the JAK–STAT pathway in RA/MPNs and cardiovascular risk and on the potential cardiovascular effects of JAK–STAT inhibitors. The JAK–STAT pathway sustains inflammatory and thrombotic events in autoimmune disorders such as RA and MPNs. Here, an imbalance exists between pro- and anti-inflammatory cytokines [increased levels of interleukin (IL)-6, IL-1-?, tumour necrosis factor-?, decreased levels of IL-10] and the over-expression of some prothrombotic proteins, such as protein kinase C?, on the surface of activated platelets. This pathway also operates in atherosclerotic cardiovascular disease. JAK–STAT inhibitors may reduce cardiovascular events and related deaths in such conditions, but the potential of these agents requires more studies, especially with regard to cardiovascular safety, and particularly for potential prothrombotic effects. JAK–STAT inhibitors merit consideration to curb heightened cardiovascular risk in patients with RA and MPNs, with rigorous assessment of the potential benefits and risks.
Francois Derimay, Gerard Finet, Gilles Rioufol
doi : 10.1093/eurheartj/ehab332
European Heart Journal, Volume 42, Issue 42, 7 November 2021, Page 4401
Simon Winther, Samuel Emil Schmidt, Juhani Knuuti, Morten Bøttcher
doi : 10.1093/eurheartj/ehab336
European Heart Journal, Volume 42, Issue 42, 7 November 2021, Pages 4402–4403
Masashi Kawamura, Osamu Monta
doi : 10.1093/eurheartj/ehab436
European Heart Journal, Volume 42, Issue 42, 7 November 2021, Page 4403
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