MicroRNA-325-3p protects the heart after myocardial infarction by inhibiting RIPK3 and programmed necrosis in mice

Necroptosis in cardiovascular disease - a new therapeutic target

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The Role of MicroRNAs in Myocardial Infarction: From Molecular Mechanism to Clinical Application

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Differences in the Korea Acute Myocardial Infarction Registry Compared with Western Registries

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Ripk3 induces mitochondrial apoptosis via inhibition of FUNDC1 mitophagy in cardiac IR injury

(2017) Hao Zhou et al.   Redox Biology

Prothrombin G20210A (rs1799963) polymorphism increases myocardial infarction risk in an age-related manner: A systematic review and meta-analysis

(2017) Changlong Li et al.   Scientific Reports

Effect of in ovo administration of an adult-derived microbiota on establishment of the intestinal microbiome in chickens

(2016) Adriana A. Pedroso et al.   AMERICAN JOURNAL OF VETERINARY RESEARCH

The long noncoding RNA NRF regulates programmed necrosis and myocardial injury during ischemia and reperfusion by targeting miR-873

(2016) K Wang et al.   CELL DEATH AND DIFFERENTIATION

Angiotensinogen-M235T as a risk factor for myocardial infarction in Asian populations: a genetic association study and a bioinformatics approach

(2016) Fariba Raygan et al.   CROATIAN MEDICAL JOURNAL

CaMKII is a RIP3 substrate mediating ischemia- and oxidative stress–induced myocardial necroptosis

(2016) Ting Zhang et al.   NATURE MEDICINE

Urotensin-ⅡReceptor Antagonist SB-710411 Protects Rat Heart against Ischemia-Reperfusion Injury via RhoA/ROCK Pathway

(2016) Sheng-Yong Luo et al.   PLoS One

Profiling of differentially expressed microRNAs in arrhythmogenic right ventricular cardiomyopathy

(2016) Hongliang Zhang et al.   Scientific Reports

Screening genes associated with myocardial infarction and transverse aortic constriction using a combined analysis of miRNA and mRNA microarray

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MicroRNAs in platelet function and cardiovascular disease

(2015) David D. McManus et al.   Nature Reviews Cardiology

Role of necroptosis in the pathogenesis of solid organ injury

(2015) H Zhao et al.   Cell Death & Disease

RIP3, a kinase promoting necroptotic cell death, mediates adverse remodelling after myocardial infarction

(2014) Mark Luedde et al.   CARDIOVASCULAR RESEARCH

Autophagic program is regulated by miR-325

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Cardiomyocyte-Specific miRNA-30c Over-Expression Causes Dilated Cardiomyopathy

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MicroRNAs Expression Profiles in Cardiovascular Diseases

(2014) Elsa Bronze-da-Rocha   Biomed Research International

Toll-like Receptor 3-mediated Necrosis via TRIF, RIP3, and MLKL

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The oral cavity is not a primary source for implantable pacemaker or cardioverter defibrillator infections

(2013) Jörg Eberhard et al.   Journal of Cardiothoracic Surgery

Time-Dependent Expression Patterns of Cardiac Aquaporins Following Myocardial Infarction

(2013) Hong Zhe Zhang et al.   JOURNAL OF KOREAN MEDICAL SCIENCE

B-vitamins intake, DNA-methylation of One Carbon Metabolism and homocysteine pathway genes and myocardial infarction risk: The EPICOR study

(2013) G. Fiorito et al.   NUTRITION METABOLISM AND CARDIOVASCULAR DISEASES

Mechanisms of Cell Death in Heart Disease

(2012) Klitos Konstantinidis et al.   ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY

Mixed Lineage Kinase Domain-like Protein Mediates Necrosis Signaling Downstream of RIP3 Kinase

(2012) Liming Sun et al.   CELL

DAI/ZBP1/DLM-1 Complexes with RIP3 to Mediate Virus-Induced Programmed Necrosis that Is Targeted by Murine Cytomegalovirus vIRA

(2012) Jason W. Upton et al.   Cell Host & Microbe

Programmed Necrosis, Not Apoptosis, in the Heart

(2011) Gloria Kung et al.   CIRCULATION RESEARCH

Nucleostemin-like 1 is required for embryogenesis and leaf development in Arabidopsis

(2011) Xiaomin Wang et al.   PLANT MOLECULAR BIOLOGY

MicroRNAs miR-1, miR-133a, miR-133b and miR-208 Are Dysregulated in Human Myocardial Infarction

(2009) Emanuela Boštjančič et al.   CARDIOLOGY

Receptor Interacting Protein Kinase-3 Determines Cellular Necrotic Response to TNF-α

(2009) Sudan He et al.   CELL

DAI/ZBP1 recruits RIP1 and RIP3 through RIP homotypic interaction motifs to activate NF-κB

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