Atherosclerosis articles within Nature Communications

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  • Article
    | Open Access

    Specialized pro-resolving mediators (SPM) are involved in the reprogramming of immune responses. Here the authors show that resolvin (RvT) 4 limits the progression of vascular disease in mouse models of arthritis exacerbated atherosclerotic inflammation.

    • Mary E. Walker
    • , Roberta De Matteis
    •  & Jesmond Dalli

  • Article
    | Open Access

    Accumulation of lipid-laden macrophages in the arterial wall is a critical step in atherosclerosis. Here, the authors show that downregulation of Zeb1 in macrophages promotes lipid accumulation and atherosclerotic plaque formation while its restoration with macrophage-targeted nanoparticles reverses these effects.

    • M. C. Martinez-Campanario
    • , Marlies Cortés
    •  & Antonio Postigo

  • Article
    | Open Access

    Hypercholesterolemia and vascular inflammation both contribute to the pathogenesis of atherosclerosis, but how hypercholesterolemia initiates vascular inflammation is not fully understood. Here the authors report that crosstalk between macrophages and endothelial cells mediated by the cholesterol metabolite 27-hydroxycholesterol drives vascular inflammation and contributes to atherosclerosis in male mice.

    • Liming Yu
    • , Lin Xu
    •  & Philip W. Shaul

  • Article
    | Open Access

    Vascular smooth muscle cells (VSMCs) are known for their fate plasticity in atherosclerosis plaque progression. Here, Zhai et al. show that extracellular traps generated from CD68 + VSMCs adversely contribute to plaque progression and highlight their unexpected role in plaque stability by regulating the direction of VSMC trans-differentiation.

    • Ming Zhai
    • , Shiyu Gong
    •  & Wenhui Peng

  • Article
    | Open Access

    Maintaining optimal eNOS levels is important during cardiovascular events, although little is known regarding the mechanism of eNOS protection. Here, the authors show a regulatory role of endothelial OASL1 in maintaining eNOS mRNA stability and vascular biology under atheroprone conditions.

    • Tae Kyeong Kim
    • , Sejin Jeon
    •  & Goo Taeg Oh

  • Article
    | Open Access

    Cholesterol efflux is mediated by specific transporters in T cells. Here the authors show that when the ABCA1/ABCG1 cholesterol transporters are absent, peripheral T cell numbers are reduced but activation increased with a premature aging phenotype of T cell senescence and apoptosis in middle aged Ldlr−/− mice.

    • Venetia Bazioti
    • , Anouk M. La Rose
    •  & Marit Westerterp

  • Article
    | Open Access

    The contribution of distinct subsets of macrophages to atherosclerosis is poorly understood. Here the authors describe a protective subset of vascular macrophages expressing the C-type lectin receptor CLEC4A2, which licenses monocytes to join the resident vascular macrophage pool and ensures vascular homeostasis.

    • Inhye Park
    • , Michael E. Goddard
    •  & Claudia Monaco

  • Article
    | Open Access

    Previous studies have shown that the CD40L-CD40 signaling axis plays a role in atherosclerosis. Here the authors investigate the cell-specific functions of the most relevant CD40L-expressing cell types in atherosclerosis. Deficiency of T cell-derived CD40L reduces and stabilizes plaques through impaired Th1 polarization while platelet-derived CD40L ameliorates atherothrombosis.

    • Michael Lacy
    • , Christina Bürger
    •  & Esther Lutgens

  • Article
    | Open Access

    Hypercholesterolemia is associated with lipid peroxidation induced reactive dicarbonyl adducts. Here the authors show that the dicarbonyl scavenger, 2-hydroxybenzylamine(2-HOBA), decreases reactive dicarbonyl modifications of LDL and HDL, improves HDL function, reduces atherosclerosis and promotes features of stable plaques in a mouse model of hypercholestrolemia.

    • Huan Tao
    • , Jiansheng Huang
    •  & MacRae F. Linton

  • Article
    | Open Access

    Endothelial cell (EC) dysfunction and inflammation contribute to plaque destabilization in atherosclerosis, increasing the risk of thrombotic events. Here, the authors show that epsin promotes EC inflammation via a mechanism involving IP3R1 degradation, and that deletion of epsin in the endothelium prevents EC dysfunctoin and atherosclerosis in mice.

    • Yunzhou Dong
    • , Yang Lee
    •  & Hong Chen

  • Article
    | Open Access

    SGLT2 inhibitors, a class of type 2 diabetes medication, reduce cardiovascular events in patients beyond expectation from blood sugar control. Here the authors report a randomized controlled trial showing that SGLT2 inhibitors reduce inflammasome activation in peripheral macrophages, which may contribute to the cardiovascular protection.

    • So Ra Kim
    • , Sang-Guk Lee
    •  & Yong-ho Lee

  • Article
    | Open Access

    The role of neutrophils in the development of atherosclerosis has long been an enigma, with few neutrophils detected within the plaque. Here, the authors show that microvesicles released from neutrophils increase vascular inflammation and enhance atherosclerotic plaque formation through delivery of miR-155.

    • Ingrid Gomez
    • , Ben Ward
    •  & Victoria Ridger

  • Article
    | Open Access

    Na+-H+ exchanger 1 (Nhe1) regulates extracellular pH by extruding protons in exchange for extracellular Na+ . Here, Liu et al. show that Nhe1 promotes the development and acidification of atherosclerotic lesions and that pH-sensitive probes can be used to monitor plaque growth and acidification.

    • Cong-Lin Liu
    • , Xian Zhang
    •  & Guo-Ping Shi

  • Article
    | Open Access

    Atherosclerosis results from the accumulation of lipoproteins in the vascular wall. Here, Thierer et al. report the design of a chemiluminescent reporter for atherogenic lipoproteins using fusion of apolipoprotein-B to a luciferase enzyme, and find it bears potential for the identification of regulators of lipoprotein metabolism in vivo.

    • James H. Thierer
    • , Stephen C. Ekker
    •  & Steven A. Farber

  • Article
    | Open Access

    Men and women differ in their risk of developing coronary artery disease, in part due to differences in their levels of sex hormones. Here, AlSiraj et al. show that the XX sex genotype regulates lipid metabolism and promotes atherosclerosis independently of sex hormones in mice.

    • Yasir AlSiraj
    • , Xuqi Chen
    •  & Lisa A. Cassis

  • Article
    | Open Access

    In atherosclerotic plaques, transformation of macrophages into foam cells is a key step in initiating the inflammatory response. Here Fan et al. show that casein kinase 2-interacting protein-1 (CKIP-1) limits foam cell formation and atherosclerosis by preventing expression of the scavenger receptor LOX-1 through REGγ-mediated degradation of Oct-1.

    • Jiao Fan
    • , Lifeng Liu
    •  & Lingqiang Zhang

  • Article
    | Open Access

    Increased glycolysis and inflammatory responses have been observed in endothelial cells exposed to disturbed flow. However, the role of endothelial glycolysis in atherosclerosis is unclear. Here the authors unveil a protective role for glycolysis by showing that endothelial deletion of Prkaa1 accelerates atherosclerosis in hyperlipidemic mice through a reduction of glycolytic metabolism.

    • Qiuhua Yang
    • , Jiean Xu
    •  & Yuqing Huo

  • Article
    | Open Access

    Vascular smooth muscle cell (VSMC) accumulation is associated with cardiovascular disease. Here, the authors combine single-cell RNA sequencing with lineage labelling to profile VSMC heterogeneity in healthy mice. They show that upregulation of Sca1 in a rare VSMC subpopulation marks a cell phenotype that is prevalent in disease.

    • Lina Dobnikar
    • , Annabel L. Taylor
    •  & Helle F. Jørgensen

  • Article
    | Open Access

    Circulating lipoprotein(a) is an important risk factor for cardiovascular disease and shows variability between different ethnic groups. Here, Zekavat et al. perform whole-genome sequencing in individuals of European and African ancestries and find ancestry-specific genetic determinants for lipoprotein(a) levels.

    • Seyedeh M. Zekavat
    • , Sanni Ruotsalainen
    •  & Sebastian Zoellner

  • Article
    | Open Access

    During atherosclerosis, endothelial cells release purines in response to oxidized phospholipids. Here, Hitzel et al. show that oxidized phospholipids activate an MTHFD2-regulated gene network in endothelial cells which reprograms amino acid metabolism towards production of purines and thus compensates for their loss.

    • Juliane Hitzel
    • , Eunjee Lee
    •  & Ralf P. Brandes

  • Article
    | Open Access

    Atherosclerosis and osteoporosis are epidemiologically associated, and oxidation specific epitopes (OSEs), which can be neutralized by innate antibodies, are pathogenic for both. Here, the authors show that mice expressing antibody fragments targeted to OSEs are protected from the bone loss induced by high-fat diet and have increased bone mass when fed a normal diet, and that levels of innate antibodies to OSEs decrease with ageing.

    • Elena Ambrogini
    • , Xuchu Que
    •  & Robert L. Jilka

  • Article
    | Open Access

    Matrix metalloproteinases (MMP) are involved in vascular remodeling associated with plaque progression. Little is known about their immune regulatory role in vascular disorders. Here, the authors report that MT4-MMP-deficiency increases the recruitment of patrolling monocytes to early atherosclerotic lesions, which accelerates atherosclerosis.

    • Cristina Clemente
    • , Cristina Rius
    •  & Alicia G. Arroyo

  • Article
    | Open Access

    Capsaicin prevents atherosclerotic plaque formation by activating TRPV1 cation channels, but its toxicity precludes its use in clinical settings. Here, Tang and colleagues use copper sulfide nanoparticles as a photothermal switch to locally and temporally activate TRPV1 in vascular smooth muscle cells and reduce plaque formation without apparent toxicity.

    • Wen Gao
    • , Yuhui Sun
    •  & Bo Tang

  • Article
    | Open Access

    The arterial wall is subjected to mechanical forces that modulate endothelial cell responses. Here, Mack and colleagues identify a novel role for Notch1 as a mechanosensor in adult arteries, where it ensures junctional integrity through modulation of calcium signalling and limits atherosclerosis.

    • Julia J. Mack
    • , Thiago S. Mosqueiro
    •  & M. Luisa Iruela-Arispe

  • Article
    | Open Access

    Atherosclerosis is characterized by subendothelial lipid retention believed to be the result of endothelial trancytosis. Here, the authors show that endothelium can take up and process LDL, generating cholesterol crystals that are deposited on the basolateral side of the cells, causing their dysfunction that can be prevented by forskolin/rolipram treatment.

    • Yvonne Baumer
    • , Sara McCurdy
    •  & William A. Boisvert

  • Article
    | Open Access

    GPCRs are key regulators of vascular functions. By analysing single-cell GPCRs expression in vascular smooth muscle and endothelial cells from healthy and diseased murine vessels, Kauret al. show that GPCR expression is highly heterogeneous in all cell types and that disease causes GPCR repertoire changes depending on cell type and vascular localization.

    • H. Kaur
    • , J. Carvalho
    •  & N. Wettschureck

  • Article
    | Open Access

    Dysfunction of autophagy in plaque macrophages aggravates atherosclerosis. Here the authors show that induction of macrophage autophagy–lysosomal biogenesis either genetically by overexpression of the master transcriptional regulator of this process, TFEB, or pharmacologically with trehalose is atheroprotective.

    • Ismail Sergin
    • , Trent D. Evans
    •  & Babak Razani

  • Article
    | Open Access

    Type-2 innate lymphoid cells (ILC2) affect adipose tissue metabolism and function. Here the authors show that the ILC2 are present in para-aortic adipose tissue and represent a major source of IL-5 and IL-13 required for mounting atheroprotective immunity, which can be altered by high fat diet.

    • Stephen A. Newland
    • , Sarajo Mohanta
    •  & Ziad Mallat

  • Review Article
    | Open Access

    Vascular endothelium possesses remarkable plasticity in response to cues from its surroundings, leading to great heterogeneity of endothelial cells in different vascular beds. Here the authors explain the molecular basis of endothelial plasticity during embryogenesis and in various diseases.

    • Elisabetta Dejana
    • , Karen K. Hirschi
    •  & Michael Simons

  • Article
    | Open Access

    Statins are lipid-lowering drugs that prevent cardiovascular disease but tolerability is limited by severe side effects in muscles. Here the authors elucidate a liver-specific activation mechanism for bempedoic acid, a novel cholesterol-lowering drug, and show how it effectively reduces LDL-C and atherosclerotic burden in mice, but does not cause myotoxicty.

    • Stephen L. Pinkosky
    • , Roger S. Newton
    •  & Narendra D. Lalwani

  • Article
    | Open Access

    Atherosclerosis is caused by low-density lipoprotein (LDL) buildup in the vessel wall, a process thought to be mediated by LDL receptor alone. Here, the authors show that the endothelium can uptake LDL via ALK1, a TGFβ signalling receptor, suggesting new therapies for blocking LDL accumulation in the vessel wall.

    • Jan R. Kraehling
    • , John H. Chidlow
    •  & William C. Sessa

  • Article
    | Open Access

    TREM-1 is a receptor that amplifies acute pro-inflammatory responses in infection. Here the authors show that TREM-1 plays an important role in atherosclerosis, a chronic and non-infectious disease, by critically skewing myelopoiesis towards preferential monocyte differentiation and by contributing to CD36-driven cellular lipid accumulation.

    • Daniel Zysset
    • , Benjamin Weber
    •  & Christoph Mueller

  • Article
    | Open Access

    Bmal1 is a key transcription factor that controls rhythmicity of diverse biological functions. Here, Pan et al. show that Bmal1 deficiency in mice increases lipoprotein secretion and reduces cholesterol excretion to bile, and decipher the molecular mechanisms underlying hyperlipidaemia and atherosclerosis promoted by the lack of Bmal1.

    • Xiaoyue Pan
    • , Christopher A. Bradfield
    •  & M. Mahmood Hussain

  • Article
    | Open Access

    Atherosclerosis progression is linked to inflammatory processes in the blood vessel wall. Here, the authors show that, with the progression of atherosclerosis, the resolution of inflammation is impaired as the result of an imbalance between specialized pro-resolving lipid mediators and leukotrienes.

    • Gabrielle Fredman
    • , Jason Hellmann
    •  & Ira Tabas

  • Article
    | Open Access

    Bone marrow cells producing the intermediate filament nestin guide monocyte egress to the bloodstream in response to infection. Here, the authors show that nestin-producing stromal cells direct inflammatory cell migration in atherosclerosis, and that stromal Mcp1 is crucial in this process.

    • Raquel del Toro
    • , Raphael Chèvre
    •  & Simón Méndez-Ferrer

  • Article
    | Open Access

    Angiopoietin-like 4 protein (ANGPTL4) is a regulator of lipoprotein metabolism whose role in atherosclerosis has been controversial. Here the authors show that ANGPTL4 deficiency in haematopoietic cells increases atherogenesis by promoting myeloid progenitor cell expansion and differentiation, foam cell formation and vascular inflammation.

    • Binod Aryal
    • , Noemi Rotllan
    •  & Carlos Fernández-Hernando

  • Article
    | Open Access

    Endothelial to mesenchymal transition (EndMT) is a crucial developmental process that also plays a role in the pathogenesis of some diseases. Here the authors show that EndMT contributes to the development of atherosclerosis in mice and humans, and is associated with complex human plaques that may be prone to rupture.

    • Solene M. Evrard
    • , Laura Lecce
    •  & Jason C. Kovacic

  • Article
    | Open Access

    The RNAse III endonuclease Dicer is crucial for processing of pre-miRNAs in health and disease. Here the authors show that endothelial Dicer promotes atherosclerosis by increasing miR-103 levels leading to suppression of the anti-inflammatory transcription factor KLF4, thus suggesting a novel approach to treat this disease.

    • Petra Hartmann
    • , Zhe Zhou
    •  & Andreas Schober

  • Article
    | Open Access

    Atherosclerosis is an inflammatory disease with limited therapeutic options. Here, the authors show that protein kinase MAP4K4 regulates vascular inflammation underlying atherosclerotic plaque development and that its inhibition prevents the disease and promotes lesion regression in mice, proposing a new atherosclerosis treatment.

    • Rachel J. Roth Flach
    • , Athanasia Skoura
    •  & Michael P. Czech

  • Article |

    Platelet-derived growth factor (PDGF) signaling in vascular smooth muscle cells (VSMCs) promotes atherogenesis. Here, the authors show that mutant mice with increased PDGF activity in VSMCs have augmented STAT1-dependent chemokine signals resulting in artery wall inflammation and formation of advanced plaque morphologies clinically relevant in humans.

    • Chaoyong He
    • , Shayna C. Medley
    •  & Lorin E. Olson

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