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The past decade has seen a marked expansion in the understanding of the pathobiology of acute myocardial infarction and the systemic inflammatory response that it elicits. At the same time, a portfolio of tools has emerged to characterise some of these processes in vivo. However, in clinical practice, key decision making still largely relies on assessment built around the timing of the onset of chest pain, features on electrocardiograms and measurements of plasma troponin. Better understanding the heterogeneity of myocardial injury and patient-level responses should provide new opportunities for diagnostic stratification to enable the delivery of more rational therapies. Characterisation of the myocardium using emerging imaging techniques such as the T1, T2 and T2* mapping techniques can provide enhanced assessments of myocardial statuses. Physiological measures, which include microcirculatory resistance and coronary flow reserve, have been shown to predict outcomes in AMI and can be used to inform treatment selection. Functionally informative blood biomarkers, including cellular transcriptomics; microRNAs; extracellular vesicle analyses and soluble markers, all give insights into the nature and timing of the innate immune response and its regulation in acute MI. The integration of these and other emerging tools will be key to developing a fuller understanding of the patient-level processes of myocardial injury and repair and should fuel new possibilities for rational therapeutic intervention.
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http://dx.doi.org/10.3390/jcm12144668 | DOI Listing |
Apoptosis
September 2025
Key Laboratory of Emergency and Trauma of the Ministry of Education, Department of Interventional Radiology and Vascular Surgery, First Affiliated Hospital of Hainan Medical University, Hainan Medical University, 31 Longhua Road, Longhua District, Haikou City, Hainan Province, China.
The singular forms of programmed cell death (PCD), including pyroptosis, apoptosis, and necroptosis, are inadequate for comprehensively elucidating the complex pathological mechanisms underlying ischemic diseases. PANoptosis is a unique lytic, innate immune, and inflammatory cell death pathway, initiated by innate immune sensors and driven by caspases and RIPKs through PANoptosome complexes. In diseases like cerebral ischemia, retinal ischemia, myocardial ischemia, renal ischemia, and spinal cord ischemia, targeting key regulatory factors of PANoptosis can help mitigate tissue damage.
View Article and Find Full Text PDFEur J Pharmacol
September 2025
Department of Cardiovascular Surgery, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University. Electronic address:
Purpose: Ischemia-reperfusion injury remains a major problem following myocardial infarction. Alpinetin (ALPT) has been reported to exhibit cardioprotective effects as well as resistance to ischemia-reperfusion injury. However, its role and mechanism during myocardial ischemia-reperfusion injury are unknown.
View Article and Find Full Text PDFBiomaterials
August 2025
Department of Anesthesiology and Perioperative Medicine, The Second Affiliated Hospital of Anhui Medical University, 678 Furong Road, Hefei, 230601, China; Key Laboratory of Anesthesiology and Perioperative Medicine of Anhui Higher Education Institutes, Anhui Medical University, 678 Furong Road, Hef
Activation of p38 mitogen-activated protein kinase plays an important role in the progression of ventricular muscle inflammation after myocardial ischemia-reperfusion (MI/R). The inhibition of p38 activation in ischemic myocardium can reduce ventricular muscle remodeling post-MI. However, owing to the dynamic change of p38 in ischemic myocardium after MI, the clinical therapeutic effect of p38 inhibitors is insufficient.
View Article and Find Full Text PDFAdv Sci (Weinh)
September 2025
Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060, P. R. China.
Mitigating myocardial ischemia-reperfusion (IR) injury is essential for enhancing the success of heart transplantation (HT) and improving patient outcomes. During HT, infiltrating neutrophils are influenced and regulated by various other cell types, contributing to myocardial IR injury through the excessive release of neutrophil extracellular traps (NETs). Nonetheless, the precise mechanisms underlying the interactions between neutrophils and other non-cardiomyocytes remain largely unexplored.
View Article and Find Full Text PDFFASEB J
September 2025
Department of Aerospace and Mechanical Engineering, University of Southern California, Los Angeles, California, USA.
Myocardial infarction (MI) is a leading cause of death worldwide and the most common precursor to heart failure, even after initial treatment. Precise evaluation of myocardial injury is crucial for assessing interventions and improving outcomes. Extensive evidence from both preclinical models and clinical studies demonstrates that the extent and severity of myocardial injury (i.
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