OOIR: Observatory of International Research

Papers

(The H4-Index of Basic Research in Cardiology is 32. The table below lists those papers that are above that threshold based on CrossRef citation counts [max. 250 papers]. The publications cover those that have been published in the past four years, i.e., from 2020-04-01 to 2024-04-01.)

Article	Citations
COVID-19 in the heart and the lungs: could we “Notch” the inflammatory storm?	152
Resolving the intertwining of inflammation and fibrosis in human heart failure at single-cell level	87
Small extracellular vesicles obtained from hypoxic mesenchymal stromal cells have unique characteristics that promote cerebral angiogenesis, brain remodeling and neurological recovery after focal cere	79
Microvascular and lymphatic dysfunction in HFpEF and its associated comorbidities	76
IMproving Preclinical Assessment of Cardioprotective Therapies (IMPACT) criteria: guidelines of the EU-CARDIOPROTECTION COST Action	72
Reduced reticulum–mitochondria Ca2+ transfer is an early and reversible trigger of mitochondrial dysfunctions in diabetic cardiomyopathy	72
Increased RyR2 activity is exacerbated by calcium leak-induced mitochondrial ROS	70
Cellular and mitochondrial mechanisms of atrial fibrillation	62
CARD9 promotes autophagy in cardiomyocytes in myocardial ischemia/reperfusion injury via interacting with Rubicon directly	61
PCSK9 regulates pyroptosis via mtDNA damage in chronic myocardial ischemia	55
Vascular autophagy in health and disease	54
Perspective: cardiovascular disease and the Covid-19 pandemic	52
Non-coding RNAs: emerging players in cardiomyocyte proliferation and cardiac regeneration	48
Cytokines as therapeutic targets for cardio- and cerebrovascular diseases	48
Mouse models of atherosclerosis and their suitability for the study of myocardial infarction	47
Hyperglycemia regulates cardiac K+ channels via O-GlcNAc-CaMKII and NOX2-ROS-PKC pathways	44
Coronary blood flow in heart failure: cause, consequence and bystander	44
Protective effect of HINT2 on mitochondrial function via repressing MCU complex activation attenuates cardiac microvascular ischemia–reperfusion injury	43
Does remote ischaemic conditioning reduce inflammation? A focus on innate immunity and cytokine response	41
Allogeneic cardiosphere-derived cells (CAP-1002) in critically ill COVID-19 patients: compassionate-use case series	41
Mitochondrial calpain-1 activates NLRP3 inflammasome by cleaving ATP5A1 and inducing mitochondrial ROS in CVB3-induced myocarditis	39
Neuraminidase-1 promotes heart failure after ischemia/reperfusion injury by affecting cardiomyocytes and invading monocytes/macrophages	39
Inflammation shapes pathogenesis of murine arrhythmogenic cardiomyopathy	38
Inhibition of macrophage proliferation dominates plaque regression in response to cholesterol lowering	37
Regulation of STAT3 and its role in cardioprotection by conditioning: focus on non-genomic roles targeting mitochondrial function	37

NAD+ administration decreases microvascular damage following cardiac ischemia/reperfusion by restoring autophagic flux	37
Plasminogen activator inhibitor-1 reduces cardiac fibrosis and promotes M2 macrophage polarization in inflammatory cardiomyopathy	35
Nuclear localization of a novel calpain-2 mediated junctophilin-2 C-terminal cleavage peptide promotes cardiomyocyte remodeling	35
Anaemia is associated with severe RBC dysfunction and a reduced circulating NO pool: vascular and cardiac eNOS are crucial for the adaptation to anaemia	35
Remote ischemic preconditioning reduces myocardial ischemia–reperfusion injury through unacylated ghrelin-induced activation of the JAK/STAT pathway	35
Cardiomyocyte Na+ and Ca2+ mishandling drives vicious cycle involving CaMKII, ROS, and ryanodine receptors	34
Fibroblast GATA-4 and GATA-6 promote myocardial adaptation to pressure overload by enhancing cardiac angiogenesis	34
Targeting myocardial ischaemic injury in the absence of reperfusion	32
miR-106a–363 cluster in extracellular vesicles promotes endogenous myocardial repair via Notch3 pathway in ischemic heart injury	32
Glucagon-like peptide-1 (GLP-1) receptor activation dilates cerebral arterioles, increases cerebral blood flow, and mediates remote (pre)conditioning neuroprotection against ischaemic stroke	32