Acute coronary syndromes articles within Nature Communications

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• Article
  27 March 2024 | Open Access

  S100A8/A9 as a prognostic biomarker with causal effects for post-acute myocardial infarction heart failure

  Heart failure is the most prevalent complication of acute myocardial infarction. Here, the authors show that circulating S100A8/A9 is a robust predictor and potentially causal medicator for heart failure post-acute myocardial infarction, as such could serve as a promising drug target for cardioprotection.

  • Jie Ma
  • , Yang Li
  •  & Yulin Li

• Article
  23 February 2024 | Open Access

  Protective effects of Pt-N-C single-atom nanozymes against myocardial ischemia-reperfusion injury

  Nanozymes can be used for targeting reactive oxygen species (ROS) to alleviate myocardial ischemia/reperfusion (I/R) injury, but hindered by catalytic performance and toxicity concerns. Here the authors report multienzyme-mimicking and biocompatible Pt-NC single-atom nanozymes as an efficient ROS decomposer for restoring cellular homeostasis and mitigating apoptotic progression after I/R injury.

  • Tianbao Ye
  • , Cheng Chen
  •  & Chengxing Shen

• Article
  21 December 2023 | Open Access

  Spatiotemporal signaling underlies progressive vascular rarefaction in myocardial infarction

  Enhancing vascularization to improve cardiac disease outcomes is a therapeutic approach with limited success. Here, the authors show that cardiac repair is governed by spatiotemporally regulated programs and underline the signaling mechanisms driving vascular deterioration.

  • Lin Wei Tung
  • , Elena Groppa
  •  & Fabio Rossi

• Article
  20 November 2023 | Open Access

  Protective effects of macrophage-specific integrin α5 in myocardial infarction are associated with accentuated angiogenesis

  During myocardial infarction, cardiac macrophages expand, become activated and play an important role in cardiac repair and remodelling. Here the authors show that integrin α5 is upregulated in infarct macrophages and contributes to myocardial repair, triggering an angiogenic phenotype and protecting from adverse remodelling.

  • Ruoshui Li
  • , Bijun Chen
  •  & Nikolaos G. Frangogiannis

• Article
  09 November 2023 | Open Access

  Gut butyrate-producers confer post-infarction cardiac protection

  Here, Chen et. al. characterize the relationship between the gut microbiota and plasma metabolite changes in the context of ST-elevation myocardial infarction (STEMI), unveiling a role of butyrate-producing bacteria and their ketogenesis in post-STEMI cardiac repair, a finding validated in nonhuman primate and mouse models. They show that butyrate supplementation reduces myocardial infarction severity in mice, underscoring the significance of butyrate-producing bacteria and beta-hydroxybutyrate in improving post-MI outcomes.

  • Hung-Chih Chen
  • , Yen-Wen Liu
  •  & Patrick C. H. Hsieh

• Article
  08 June 2023 | Open Access

  SERCA2 phosphorylation at serine 663 is a key regulator of Ca²⁺ homeostasis in heart diseases

  Despite advances in cardioprotection, new therapeutic strategies precluding ischemia-reperfusion injury of patients are still needed. Here, the authors show that preventing serine 663 phosphorylation of SERCA2, significantly increases its activity and protects against cell death, by counteracting cytosolic and mitochondrial Ca²⁺ overload.

  • Fabrice Gonnot
  • , Laura Boulogne
  •  & Ludovic Gomez

• Article
  10 December 2022 | Open Access

  Targeting cardiomyocyte ADAM10 ectodomain shedding promotes survival early after myocardial infarction

  Therapeutic interference with the immune response after myocardial infarction holds the potential to close a clinically relevant gap. Here, the authors show that inhibition of a cardiomyocyte-specific ADAM10 / CX3CL1 axis improves post infarction survival and cardiac function by attenuating neutrophil-mediated myocardial damage.

  • Erik Klapproth
  • , Anke Witt
  •  & Ali El-Armouche

• Article
  06 December 2022 | Open Access

  Extracellular traps from activated vascular smooth muscle cells drive the progression of atherosclerosis

  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
  06 October 2021 | Open Access

  Multi-targeted ¹H/¹⁹F MRI unmasks specific danger patterns for emerging cardiovascular disorders

  The prediction of major cardiovascular events is still an unsolved problem. Here, the authors present a multi-color, multi-targeted non-invasive imaging technology that allows reliable in vivo identification of silent but prognostically highly relevant danger patterns prior to myocardial infarction in mice.

  • Ulrich Flögel
  • , Sebastian Temme
  •  & Bodo Levkau

• Article
  23 July 2021 | Open Access

  Nitrate-functionalized patch confers cardioprotection and improves heart repair after myocardial infarction via local nitric oxide delivery

  Nitric oxide (NO) is an important gaseous signaling molecule with multiple physiological roles in cardiovascular system. Here the authors develop a cardiac patch with NO releasing function that favors heart repair after myocardial infarction.

  • Dashuai Zhu
  • , Jingli Hou
  •  & Qiang Zhao

• Article
  22 January 2021 | Open Access

  The long noncoding RNA lncCIRBIL disrupts the nuclear translocation of Bclaf1 alleviating cardiac ischemia–reperfusion injury

  Cardiac ischemia–reperfusion (I/R) injury represents a key threat to human health. This study reveals that the long noncoding RNA lncRNA-CIRBIL is protective against I/R injury by inhibiting the nuclear translocation of Bclaf1.

  • Yang Zhang
  • , Xiaofang Zhang
  •  & Zhenwei Pan

• Article
  04 January 2021 | Open Access

  Cardiomyocytes stimulate angiogenesis after ischemic injury in a ZEB2-dependent manner

  ZEB2 transcription factor is increased in a subset of cardiomyocytes during stress to induce cardioprotective effects after injury. Here the authors show that therapeutic delivery of ZEB2 prevents cardiac dysfunction after ischemic damage and promotes the activation of pro-angiogenic signals.

  • Monika M. Gladka
  • , Arwa Kohela
  •  & Eva van Rooij

• Article
  20 October 2020 | Open Access

  CHIP phosphorylation by protein kinase G enhances protein quality control and attenuates cardiac ischemic injury

  Carboxyl terminus of Hsc70-interacting protein (CHIP) is proteostasis regulator. Here the authors show that CHIP-mediated protein turnover is enhanced by PKG-mediated phosphorylation, which results in attenuated cardiac ischemic proteotoxicity.

  • Mark J. Ranek
  • , Christian Oeing
  •  & David A. Kass

• Article
  07 August 2020 | Open Access

  Machine learning-based prediction of acute coronary syndrome using only the pre-hospital 12-lead electrocardiogram

  Diagnosing a heart attack requires excessive testing and prolonged observation, which frequently requires hospital admission. Here the authors report a machine learning-based system based exclusively on ECG data that can help clinicians identify 37% more heart attacks during initial screening.

  • Salah Al-Zaiti
  • , Lucas Besomi
  •  & Ervin Sejdić

• Article
  29 June 2020 | Open Access

  Iron imaging in myocardial infarction reperfusion injury

  Restoration of coronary blood flow after a heart attack may lead to reperfusion injury and pathologic iron deposition. Here, the authors perform magnetic susceptibility imaging showing its association with iron in a large animal model of myocardial infarction during wound healing, and showing feasibility in acute myocardial infarction patients undergoing percutaneous coronary intervention.

  • Brianna F. Moon
  • , Srikant Kamesh Iyer
  •  & Walter R. Witschey

• Article
  03 April 2020 | Open Access

  Diagnosis and prognosis of myocardial infarction on a plasmonic chip

  The gold standard for diagnosis and monitoring of myocardial infarction is a chemiluminescence assay based on the detection of cardian troponin I (cTnI). Here, the authors develop a plasmonic gold nano-island chip assay for ultrasensitive detection of cTnI in as little as 10 μL of serum.

  • Wei Xu
  • , Lin Wang
  •  & Kun Qian

• Article
  11 March 2020 | Open Access

  Red blood cell-derived semaphorin 7A promotes thrombo-inflammation in myocardial ischemia-reperfusion injury through platelet GPIb

  Reperfusion injury following myocardial ischemia is aggravated by inflammation and platelet–neutrophil complex formation. Here the authors show that semaphorin 7A binds to platelet GPIb, enhancing platelet–neutrophil interaction and increasing post-ischemic myocardial tissue injury, and that blockage of semaphorin 7A is protective.

  • David Köhler
  • , Tiago Granja
  •  & Peter Rosenberger

• Article
  20 September 2019 | Open Access

  Circular RNA CircFndc3b modulates cardiac repair after myocardial infarction via FUS/VEGF-A axis

  Circular RNAs (circRNAs) are non-coding RNAs generated from pre-mRNAs of coding genes by the splicing machinery whose function in the heart is poorly understood. Here the authors show that AAV-mediated delivery of the circRNA circFndc3b prevents cardiomyocyte apoptosis, enhances angiogenesis, and attenuates LV dysfunction post-MI in mice by regulating FUS-VEGF-A signalling.

  • Venkata Naga Srikanth Garikipati
  • , Suresh Kumar Verma
  •  & Raj Kishore

• Article
  09 July 2019 | Open Access

  Identification of a pro-angiogenic functional role for FSP1-positive fibroblast subtype in wound healing

  Activated fibroblasts are key contributors to tissue repair after cardiac injury. Here, Saraswati et al. identify and characterize a subpopulation of FSP1-positive cardiac fibroblasts with proangiogenic properties in infarcted hearts.

  • Sarika Saraswati
  • , Stephanie M. W. Marrow
  •  & Pampee P. Young

• Article
  24 May 2019 | Open Access

  Contemporaneous 3D characterization of acute and chronic myocardial I/R injury and response

  Detailed characterization of cardiac damage following ischemia/reperfusion injury and detection of occurring inflammatory responses is important for the development of new therapeutic concepts. Here the authors present a method for the three-dimensional investigation of acute and chronic cardiac injury responses using light sheet fluorescence microscopy.

  • Simon F. Merz
  • , Sebastian Korste
  •  & Matthias Totzeck

• Article
  15 April 2019 | Open Access

  Enzyme-responsive progelator cyclic peptides for minimally invasive delivery to the heart post-myocardial infarction

  Injectable hydrogels have gained significant interest; yet, due to high viscosity, many are unsuitable for catheter delivery. Here, the authors report on cyclic peptides with low viscosity for catheter delivery, which form self-assembled peptide hydrogels following enzymatic cleavage and demonstrated delivery in vivo.

  • Andrea S. Carlini
  • , Roberto Gaetani
  •  & Nathan C. Gianneschi

• Article
  26 February 2018 | Open Access

  Hypoxia-inducible factor 2-alpha-dependent induction of amphiregulin dampens myocardial ischemia-reperfusion injury

  Myocardial ischemia–reperfusion injury stabilizes the hypoxia-inducible factor HIF2-alpha. Here, the authors show that HIF2-alpha protects the heart from injury via induction of the epidermal growth factor amphiregulin, and that amphiregulin administration is cardioprotective in mice.

  • Michael Koeppen
  • , Jae W. Lee
  •  & Holger K. Eltzschig

• Correspondence
  07 February 2018 | Open Access

  Correspondence: Reply to ‘Compound 17b and formyl peptide receptor biased agonism in relation to cardioprotective effects in ischaemia-reperfusion injury’

  • Cheng Xue Qin
  • , Lauren T. May
  •  & Rebecca H. Ritchie

• Article
  10 October 2017 | Open Access

  Cardioprotection induced in a mouse model of neuropathic pain via anterior nucleus of paraventricular thalamus

  Various forms of preconditioning can prevent ischemic-reperfusion injury after myocardial infarction. Here, the authors show that in mice, the presence of chronic neuropathic pain can have a cardioprotective effect, and that this is dependent on neural activation in the paraventricular thalamus.

  • Yi-Fen Cheng
  • , Ya-Ting Chang
  •  & Chien-Chang Chen

• Article
  05 September 2017 | Open Access

  Cre/lox-assisted non-invasive in vivo tracking of specific cell populations by positron emission tomography

  Non-invasive cell tracking is a powerful method to visualize cells in vivo under physiological and pathophysiological conditions. Here Thunemann et al. generate a mouse model for in vivo tracking and quantification of specific cell types by combining a PET reporter gene with Cre-dependent activation that can be exploited for any cell population for which a Cre mouse line is available.

  • Martin Thunemann
  • , Barbara F. Schörg
  •  & Robert Feil

• Article
  13 July 2017 | Open Access

  Near-infrared autofluorescence induced by intraplaque hemorrhage and heme degradation as marker for high-risk atherosclerotic plaques

  Atherosclerosis diagnosis relies primarily on imaging and early detection of high-risk atherosclerotic plaques is important for risk stratification of patients and stabilization therapies. Here Htun et al. demonstrate that vulnerable atherosclerotic plaques generate near-infrared autofluorescence that can be detected via emission computed tomography.

  • Nay Min Htun
  • , Yung Chih Chen
  •  & Karlheinz Peter

• Article
  22 July 2016 | Open Access

  Genetic lineage tracing defines myofibroblast origin and function in the injured heart

  The origin and fate of myofibroblasts, the cells responsible for cardiac remodelling and fibrosis, is controversial. Here the authors show that cardiac myofibroblasts express periostin, derive exclusively from tissue-resident fibroblasts, are necessary for scar formation after injury, and can revert back to a less-activated state upon injury resolution.

  • Onur Kanisicak
  • , Hadi Khalil
  •  & Jeffery D. Molkentin

• Article
  10 May 2016 | Open Access

  Arrhythmia risk stratification of patients after myocardial infarction using personalized heart models

  Sudden arrhythmic death is a leading cause of mortality, however approaches to identify at-risk patients are of low sensitivity and specificity. Here, the authors develop a personalized approach to assess arrhythmia risk in post-infarction patients based on cardiac imaging and computational modelling that significantly outperforms existing clinical metrics.

  • Hermenegild J. Arevalo
  • , Fijoy Vadakkumpadan
  •  & Natalia A. Trayanova

• Article
  24 February 2016 | Open Access

  Rationally engineered Troponin C modulates in vivo cardiac function and performance in health and disease

  Heart contraction, which is decreased in disease, is determined by Ca²⁺binding to troponin C. Here, the authors combine a protein engineering approach with gene therapy to modulate heart contractility in mice with the use of rationally designed Troponin C variants, suggesting a new therapy for diseased hearts.

  • Vikram Shettigar
  • , Bo Zhang
  •  & Jonathan P. Davis

• Article | 17 July 2015

  E2F1-dependent miR-421 regulates mitochondrial fragmentation and myocardial infarction by targeting Pink1

  Inhibition of mitochondrial fragmentation can block or delay cell death. Here the authors show that the signalling axis E2F1-miR-421-Pink1 represents a major regulator of mitochondrial fission and cardiomyocyte death, identifying potential therapeutic targets for treatment of heart failure.

  • Kun Wang
  • , Lu-Yu Zhou
  •  & Pei-Feng Li

• Article | 10 April 2015

  APF lncRNA regulates autophagy and myocardial infarction by targeting miR-188-3p

  ATG7 promotes cardiomyocyte autophagy but the molecular mechanism of its regulation is unknown. Here, Wang et al.identify a long non-coding RNA dubbed autophagy promoting factor (APF) that binds and inhibits miR-188-3p, which in turn acts on ATG7, to regulate cardiac autophagy.

  • Kun Wang
  • , Cui-Yun Liu
  •  & Pei-Feng Li

• Article
  02 February 2015 | Open Access

  Targeting protein tyrosine phosphatase σ after myocardial infarction restores cardiac sympathetic innervation and prevents arrhythmias

  Chondroitin sulfate proteoglycans (CSP) in the myocardial scar inhibit the tissue’s reinnervation, rendering it prone to arrhythmia. Here the authors show that blocking the activity of the CSP receptor, protein tyrosine phosphatase receptor σ, promotes scar reinnervation and prevents arrhythmia in mice.

  • R. T. Gardner
  • , L. Wang
  •  & B. A. Habecker

• Article | 18 December 2014

  Telomerase expression confers cardioprotection in the adult mouse heart after acute myocardial infarction

  Short telomeres are risk factors for age-associated diseases such as cardiopathies. Here the authors show that cardiac reactivation of telomerase, the telomere-elongating enzyme whose expression is normally silenced postnatally, mitigates the consequences of myocardial infarction in adult mice.

  • Christian Bär
  • , Bruno Bernardes de Jesus
  •  & Maria A. Blasco

• Article
  06 June 2014 | Open Access

  Dynamic haematopoietic cell contribution to the developing and adult epicardium

  The murine epicardium forms an envelope around the heart and contains cells that can participate in cardiac repair. Here the authors discover a population of epicardial cells derived from blood cells, which proliferate and change their surrounding extracellular matrix in response to cardiac injury.

  • Gemma M. Balmer
  • , Sveva Bollini
  •  & Paul R. Riley

• Article | 07 April 2014

  CARL lncRNA inhibits anoxia-induced mitochondrial fission and apoptosis in cardiomyocytes by impairing miR-539-dependent PHB2 downregulation

  The prohibitin complex promotes cell survival by regulating mitochondrial morphogenesis. Wang et al.identify a long non-coding RNA that regulates this complex in cardiomyocytes by acting as a sponge to downregulate a prohibitin-targetting miRNA, protecting cells from apoptosis in anoxic conditions.

  • Kun Wang
  • , Bo Long
  •  & Pei-Feng Li