Research Highlights |
Featured
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Letter |
Inhibition of miR-33a/b in non-human primates raises plasma HDL and lowers VLDL triglycerides
- Katey J. Rayner
- , Christine C. Esau
- & Kathryn J. Moore
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News & Views |
Heart fails without pump partner
Mishandling of calcium ions by cardiac cells causes the heart to malfunction. The discovery of a crucial modification to a calcium pump inside the cell opens up a potential way to correct this. See Letter p.601
- Sudha K. Shenoy
- & Howard A. Rockman
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Research Highlights |
Heart attack hits bone marrow
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Inside View |
Inside View: Pfizer
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Letter |
Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk
- Georg B. Ehret
- , Patricia B. Munroe
- & Toby Johnson
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Letter |
SUMO1-dependent modulation of SERCA2a in heart failure
- Changwon Kho
- , Ahyoung Lee
- & Roger J. Hajjar
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News & Views |
Several small shocks beat one big one
Life-threatening abnormalities in the electrical rhythm of the heart are usually treated with the application of a large electric shock. An approach involving a significantly smaller shock energy may be equally effective. See Letter p.235
- Richard A. Gray
- & John P. Wikswo
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News |
A kinder, gentler defibrillator
A new technique could lower the intensity of the shock needed to reset electrical instabilities in the heart.
- Alla Katsnelson
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Letter |
Low-energy control of electrical turbulence in the heart
- Stefan Luther
- , Flavio H. Fenton
- & Eberhard Bodenschatz
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News Explainer |
Review adds salt to a familiar concern
Link between salt consumption and heart disease challenged.
- Ewen Callaway
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News & Views |
Muscle for a damaged heart
When cardiac muscle cells die during a heart attack, this can lead to heart failure and even death. It now emerges that stem cells of the 'sheet' enveloping the heart can be coaxed to form new muscle after such an event. See Letter p.640
- Vincent Christoffels
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News |
Stem cells patch up 'broken' heart
Cell reactivation in mouse hearts repairs muscle after heart attack.
- Marian Turner
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Letter |
De novo cardiomyocytes from within the activated adult heart after injury
- Nicola Smart
- , Sveva Bollini
- & Paul R. Riley
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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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News & Views |
To the rescue of the failing heart
Heart failure is characterized by weakened contractions of heart muscle. A drug that directly activates the key force-generating molecule in this muscle may be a valuable tool to strengthen the failing heart.
- Donald M. Bers
- & Samantha P. Harris
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News & Views |
The diet–microbe morbid union
A common dietary component that some people even take as a supplement is converted by the gut microbiota to harmful metabolites linked to heart disease. This finding has cautionary implications. See Article p.57
- Kimberly Rak
- & Daniel J. Rader
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Article |
Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease
This paper shows that gut flora can influence cardiovascular disease, by metabolizing a dietary phospholipid. Using a metabolomics approach it is found that plasma levels of three metabolites of dietary phosphatidylcholine—choline, betaine and TMAO—are associated with increased risk of cardiovascular disease in humans. The gut flora is known to have a role in TMAO formation from choline, and this paper shows that dietary choline supplementation enhances macrophage foam cell formation and lesion formation in atherosclerosis-prone mice, but not if the gut flora are depleted with antibiotics.
- Zeneng Wang
- , Elizabeth Klipfell
- & Stanley L. Hazen
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Research Highlights |
Clues from big-hearted mice
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Letter |
Recapitulation of premature ageing with iPSCs from Hutchinson–Gilford progeria syndrome
- Guang-Hui Liu
- , Basam Z. Barkho
- & Juan Carlos Izpisua Belmonte
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Letter |
9p21 DNA variants associated with coronary artery disease impair interferon-γ signalling response
A non-coding region on chromosome 9p21 was previously shown to associate with coronary artery disease and type 2 diabetes, and the region has been implicated in regulating neighbouring genes. Here, 33 distinct enhancers within this region are identified, showing that SNPs in one of the enhancers affect STAT1 binding. Furthermore, it is shown that in human vascular endothelial cells the enhancer interval physically interacts with a number of specific loci and that IFN-γ activation strongly affects the chromatin structure and transcriptional regulation of the 9p21 locus, including STAT1 binding, long-range enhancer interactions and expression of neighbouring genes.
- Olivier Harismendy
- , Dimple Notani
- & Kelly A. Frazer
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Research Highlights |
Fooling the heart into repair
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Review Article |
Pervasive roles of microRNAs in cardiovascular biology
- Eric M. Small
- & Eric N. Olson
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Letter |
S-glutathionylation uncouples eNOS and regulates its cellular and vascular function
The enzyme eNOS is crucial for regulating vascular function as it can produce both the vasodilator nitric oxide and the vasoconstrictor superoxide. Here it is shown that a modification associated with oxidant stress, S-glutathionylation, switches the enzyme from forming nitric oxide to forming superoxide. In hypertensive vessels, S-glutathionylation of eNOS is increased and this is associated with impaired endothelium-dependent vasodilation.
- Chun-An Chen
- , Tse-Yao Wang
- & Jay L. Zweier
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Research Highlights |
Medicine: Profiling for blood pressure
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News |
Good news for 'good' cholesterol
Positive results inject life into strategy to treat heart disease.
- Alla Katsnelson
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Research Highlights |
Vascular biology: Clot catcher
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News |
Skin cells converted to heart muscle cells
Cell identity switched in mice without the use of stem cells.
- Heidi Ledford
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Article |
From noncoding variant to phenotype via SORT1 at the 1p13 cholesterol locus
A non-coding polymorphism at a locus associated with myocardial infarction in humans creates a CCAAT/enhancer binding protein transcription factor binding site and alters the hepatic expression of the SORT1 gene. These authors show that modulating Sort1 levels in mouse liver alters levels of plasma low-density lipoprotein cholesterol and very low-density lipoprotein, potentially explaining why polymorphisms at this locus are associated with heart disease.
- Kiran Musunuru
- , Alanna Strong
- & Daniel J. Rader
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Article |
Biological, clinical and population relevance of 95 loci for blood lipids
Lipid concentration in the serum is one of the most important risk factors for coronary artery disease and can be targeted for therapeutic intervention. A genome-wide association study in >100,000 individuals of European ancestry now finds 95 significantly associated loci that also affect lipid traits in non-European populations. Among associated loci are those involved in cholesterol metabolism, known targets of cholesterol-lowering drugs and those that contribute to normal variation in lipid traits and to extreme lipid phenotypes.
- Tanya M. Teslovich
- , Kiran Musunuru
- & Sekar Kathiresan
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News & Views |
Variations in blood lipids
What is the new gold standard for genome-wide association studies? As exemplified by analyses of blood lipids, it is collaboration to amass huge sample sizes and functional studies of the genes identified.
- Alan R. Shuldiner
- & Toni I. Pollin
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Research Highlights |
Cardiovascular biology: Low B cells, low plaques
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Article |
Chromatin regulation by Brg1 underlies heart muscle development and disease
Cardiac hypertrophy is associated with a decrease in expression of the adult isoform of the molecular motor myosin heavy chain (α-MHC) and the induction of expression of its fetal isoform (β-MHC). Here the authors reveal the mechanism regulating this switch in expression, which impairs heart function. Cardiac stress in adult hearts reactivates the developmental chromatin-modifying complex Brg1/BAF, which interacts with histone deacetylase and poly (ADP ribose) polymerase to induce a pathological α-MHC-to-β-MHC shift.
- Calvin T. Hang
- , Jin Yang
- & Ching-Pin Chang
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News |
Evidence mounts against diabetes drug
Studies continue to find heart-attack risk.
- Heidi Ledford
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Letter |
Patient-specific induced pluripotent stem-cell-derived models of LEOPARD syndrome
The generation of induced pluripotent stem cells (iPSCs) from patients with defined genetic disorders promises to help the basic understanding of complex diseases and the development of therapeutics. Here iPSCs have been generated from patients with LEOPARD syndrome, a developmental disorder with pleiomorphic effects on several tissues and organs. The iPSCs are characterized and the phenotype of cardiomyocytes derived from these cells is investigated.
- Xonia Carvajal-Vergara
- , Ana Sevilla
- & Ihor R. Lemischka
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Research Highlights |
Genomics: Rat sequencing redux
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Letter |
Targeted deletion of the 9p21 non-coding coronary artery disease risk interval in mice
Sequence variations in a 58-kilobase interval on human chromosome 9p21 have been associated with an increased risk of coronary artery disease. However, this interval contains no protein-coding genes and the mechanism underlying the increased risk has been unclear. Here, the corresponding interval has been deleted from mouse chromosome 4, revealing that this part of the chromosome regulates the cardiac expression of two nearby genes, Cdkn2a and Cdkn2b, and the proliferation dynamics of vascular cells.
- Axel Visel
- , Yiwen Zhu
- & Len A. Pennacchio
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News |
Junk DNA holds clues to heart disease
Deleting a non-coding region leads to narrowing of arteries in mice.
- Janet Fang
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News & Views |
50 & 100 years ago
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Research Highlights |
Vascular biology: Hearty hormones
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News |
Bisphenol A link to heart disease confirmed
Second study supports an association between the controversial chemical and cardiovascular problems.
- Brendan Borrell
Heart regeneration
Testing time for stem cells