Featured
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Review Article |
The changing landscape of atherosclerosis
This Review discusses recent research that has transformed our understanding of the biology of atherosclerosis, and examines its implications for the treatment of atherosclerotic cardiovascular disease.
- Peter Libby
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Article |
ALDH4A1 is an atherosclerosis auto-antigen targeted by protective antibodies
An autoantibody found in a mouse model of atherosclerosis recognizses ALDH4A1, and infusion of the antibody delays plaque formation in mice.
- Cristina Lorenzo
- , Pilar Delgado
- & Almudena R. Ramiro
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Letter |
Externalized histone H4 orchestrates chronic inflammation by inducing lytic cell death
Histone H4 is released from neutrophil extracellular traps and induces membrane lysis in vascular smooth muscle cells, leading to the destabilization of atherosclerotic plaques.
- Carlos Silvestre-Roig
- , Quinte Braster
- & Oliver Soehnlein
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Letter |
SR-B1 drives endothelial cell LDL transcytosis via DOCK4 to promote atherosclerosis
The SR-B1 receptor partners with DOCK4 and RAC1 to drive the uptake and transcytosis of LDL in endothelial cells, thereby promoting atherosclerosis in mice.
- Linzhang Huang
- , Ken L. Chambliss
- & Philip W. Shaul
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Letter |
Oxidized phospholipids are proinflammatory and proatherogenic in hypercholesterolaemic mice
A single-chain variable fragment of the antibody E06, which binds to the phosphocholine headgroup of oxidized phospholipids, blocks the uptake of oxidized low-density lipoprotein by macrophages, and reduces inflammation and atherosclerosis in hypercholesterolaemic mice.
- Xuchu Que
- , Ming-Yow Hung
- & Joseph L. Witztum
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Letter |
Integrin-YAP/TAZ-JNK cascade mediates atheroprotective effect of unidirectional shear flow
YAP and TAZ, effectors of the Hippo pathway, sense mechanical forces generated by blood flow and play a role in atherosclerosis pathogenesis.
- Li Wang
- , Jiang-Yun Luo
- & Yu Huang
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Letter |
Control of mitochondrial function and cell growth by the atypical cadherin Fat1
Fragments of the atypical cadherin Fat1 accumulate in the mitochondria of vascular smooth muscle cells where they reduce respiration, leading to a regulated proliferative response to arterial injury.
- Longyue L. Cao
- , Dario F. Riascos-Bernal
- & Nicholas E. S. Sibinga
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Letter |
CD47-blocking antibodies restore phagocytosis and prevent atherosclerosis
Atherosclerotic lesions in mice and humans switch on a ‘don’t eat me’ signal—expression of CD47—that prevents effective removal of diseased tissue; anti-CD47 antibody therapy can normalize this defective efferocytosis, with beneficial results in several mouse models of atherosclerosis.
- Yoko Kojima
- , Jens-Peter Volkmer
- & Nicholas J. Leeper
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Outlook |
Cardiovascular disease: Biochemistry to behaviour
Cardiovascular disease (CVD) remains the grim reaper's primary calling card, but people can take steps to keep the world's number one killer at bay.
- Bill Cannon
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Research Highlights |
Fatty plaque link to inflammation
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News |
Animals engineered with pinpoint accuracy
More accurate genetic modification has created allergen-free cow's milk and pigs that could serve as a model for atherosclerosis.
- Amy Maxmen
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News & Views |
Bad matters made worse
Heart attacks occur when lipoprotein-driven inflammation called atherosclerosis triggers blood clotting in the arteries. It seems that the attacks can, in turn, accelerate atherosclerosis by fanning the inflammation. See Letter p.325
- Ira Tabas
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Article |
Myocardial infarction accelerates atherosclerosis
Myocardial infarction accelerates atherosclerosis through activation of the sympathetic nervous system, and the consequent release of haematopoietic stem and progenitor cells.
- Partha Dutta
- , Gabriel Courties
- & Matthias Nahrendorf
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Research Highlights |
Culprits in diabetic heart risk
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Research Highlights |
Stranded cells fuel plaques
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Review Article |
Progress and challenges in translating the biology of atherosclerosis
- Peter Libby
- , Paul M Ridker
- & Göran K. Hansson
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Research Highlights |
Cardiovascular biology: Low B cells, low plaques
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Letter |
NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals
During atherosclerosis, crystals of cholesterol accumulate in atherosclerotic plaques. But are they a consequence or a cause of the inflammation associated with the disease? Here it is shown that small cholesterol crystals appear early in the development of atherosclerosis, and that they act as an endogenous danger signal, causing inflammation by activating the NLRP3 inflammasome pathway. Cholesterol crystals thus seem to be an early cause, rather than a late consequence, of inflammation.
- Peter Duewell
- , Hajime Kono
- & Eicke Latz
Neuroimmune cardiovascular interfaces control atherosclerosis