{"entity": "journal", "iuid": "4b549d6bc68a49239143ae8f7d318aa3", "timestamp": "2026-07-13T04:04:18.354Z", "links": {"self": {"href": "https://publications.scilifelab.se/journal/Front%20Cardiovasc%20Med.json"}, "display": {"href": "https://publications.scilifelab.se/journal/Front%20Cardiovasc%20Med"}}, "title": "Front Cardiovasc Med", "issn": "2297-055X", "issn-l": null, "publications_count": 2, "publications": [{"entity": "publication", "iuid": "8e85b6ad150c4fb9a516a6851cc29b7d", "links": {"self": {"href": "https://publications.scilifelab.se/publication/8e85b6ad150c4fb9a516a6851cc29b7d.json"}, "display": {"href": "https://publications.scilifelab.se/publication/8e85b6ad150c4fb9a516a6851cc29b7d"}}, "title": "Ischemic preconditioning affects phosphosites and accentuates myocardial stunning while reducing infarction size in rats.", "authors": [{"family": "Elmahdy", "given": "Ahmed", "initials": "A"}, {"family": "Shekka Espinosa", "given": "Aaron", "initials": "A"}, {"family": "Kakaei", "given": "Yalda", "initials": "Y"}, {"family": "Pylova", "given": "Tetiana", "initials": "T"}, {"family": "Jha", "given": "Abhishek", "initials": "A"}, {"family": "Zulfaj", "given": "Ermir", "initials": "E"}, {"family": "Krasnikova", "given": "Maryna", "initials": "M"}, {"family": "Al-Awar", "given": "Amin", "initials": "A"}, {"family": "Sheybani", "given": "Zahra", "initials": "Z"}, {"family": "Sevastianova", "given": "Valentyna", "initials": "V"}, {"family": "Berger", "given": "Evelin", "initials": "E"}, {"family": "Nejat", "given": "Amirali", "initials": "A"}, {"family": "Molander", "given": "Linnea", "initials": "L"}, {"family": "Andersson", "given": "Erik Axel", "initials": "EA"}, {"family": "Omerovic", "given": "Elmir", "initials": "E"}, {"family": "Hussain", "given": "Shafaat", "initials": "S"}, {"family": "Redfors", "given": "Bj\u00f6rn", "initials": "B"}], "type": "journal article", "published": "2024-03-15", "journal": {"title": "Front Cardiovasc Med", "issn": "2297-055X", "volume": "11", "pages": "1376367", "issn-l": null}, "abstract": "Ischemic preconditioning (IPC), i.e., brief periods of ischemia, protect the heart from subsequent prolonged ischemic injury, and reduces infarction size. Myocardial stunning refers to transient loss of contractility in the heart after myocardial ischemia that recovers without permanent damage. The relationship between IPC and myocardial stunning remains incompletely understood. This study aimed primarily to examine the effects of IPC on the relationship between ischemia duration, stunning, and infarct size in an ischemia-reperfusion injury model. Secondarily, this study aimed to examine to which extent the phosphoproteomic changes induced by IPC relate to myocardial contractile function.\n\nRats were subjected to different durations of left anterior descending artery (LAD) occlusion, with or without preceding IPC. Echocardiograms were acquired to assess cardiac contraction in the affected myocardial segment. Infarction size was evaluated using triphenyl tetrazolium chloride staining. Phosphoproteomic analysis was performed in heart tissue from preconditioned and non-preconditioned animals. In contrast to rats without IPC, reversible akinesia was observed in a majority of the rats that were subjected to IPC and subsequently exposed to ischemia of 13.5 or 15 min of ischemia. Phosphoproteomic analysis revealed significant differential regulation of 786 phosphopeptides between IPC and non-IPC groups, with significant associations with the sarcomere, Z-disc, and actin binding.\n\nIPC induces changes in phosphosites of proteins involved in myocardial contraction; and both accentuates post-ischemic myocardial stunning and reduces infarct size.", "doi": "10.3389/fcvm.2024.1376367", "pmid": "38559672", "labels": {"Glycoproteomics and MS Proteomics": "Collaborative"}, "xrefs": [{"db": "pmc", "key": "PMC10978780"}], "notes": [], "created": "2024-11-27T15:32:32.338Z", "modified": "2024-11-27T15:35:23.688Z"}, {"entity": "publication", "iuid": "2ba25a8f3d6b49d3a58d4bd152746568", "links": {"self": {"href": "https://publications.scilifelab.se/publication/2ba25a8f3d6b49d3a58d4bd152746568.json"}, "display": {"href": "https://publications.scilifelab.se/publication/2ba25a8f3d6b49d3a58d4bd152746568"}}, "title": "Unraveling the Metabolic Derangements Occurring in Non-infarcted Areas of Pig Hearts With Chronic Heart Failure.", "authors": [{"family": "Correia", "given": "Cl\u00e1udia", "initials": "C"}, {"family": "Wang", "given": "Qing-Dong", "initials": "QD"}, {"family": "Linhardt", "given": "Gunilla", "initials": "G"}, {"family": "Carlsson", "given": "Leif G", "initials": "LG"}, {"family": "Ulfenborg", "given": "Benjamin", "initials": "B"}, {"family": "Walentinsson", "given": "Anna", "initials": "A"}, {"family": "Ryd\u00e9n-Markinhutha", "given": "Katarina", "initials": "K"}, {"family": "Behrendt", "given": "Margareta", "initials": "M"}, {"family": "Wikstr\u00f6m", "given": "Johannes", "initials": "J"}, {"family": "Sartipy", "given": "Peter", "initials": "P"}, {"family": "Jennbacken", "given": "Karin", "initials": "K"}, {"family": "Synnergren", "given": "Jane", "initials": "J"}], "type": "journal article", "published": "2021-10-13", "journal": {"title": "Front Cardiovasc Med", "issn": "2297-055X", "volume": "8", "pages": "753470", "issn-l": null}, "abstract": "Objective: After myocardial infarction (MI), the non-infarcted left ventricle (LV) ensures appropriate contractile function of the heart. Metabolic disturbance in this region greatly exacerbates post-MI heart failure (HF) pathology. This study aimed to provide a comprehensive understanding of the metabolic derangements occurring in the non-infarcted LV that could trigger cardiovascular deterioration. Methods and Results: We used a pig model that progressed into chronic HF over 3 months following MI induction. Integrated gene and metabolite signatures revealed region-specific perturbations in amino acid- and lipid metabolism, insulin signaling and, oxidative stress response. Remote LV, in particular, showed impaired glutamine and arginine metabolism, altered synthesis of lipids, glucose metabolism disorder, and increased insulin resistance. LPIN1, PPP1R3C, PTPN1, CREM, and NR0B2 were identified as the main effectors in metabolism dysregulation in the remote zone and were found differentially expressed also in the myocardium of patients with ischemic and/or dilated cardiomyopathy. In addition, a simultaneous significant decrease in arginine levels and altered PRCP, PTPN1, and ARF6 expression suggest alterations in vascular function in remote area. Conclusions: This study unravels an array of dysregulated genes and metabolites putatively involved in maladaptive metabolic and vascular remodeling in the non-infarcted myocardium and may contribute to the development of more precise therapies to mitigate progression of chronic HF post-MI.", "doi": "10.3389/fcvm.2021.753470", "pmid": "34722683", "labels": {"Swedish Metabolomics Centre": "Service"}, "xrefs": [{"db": "pmc", "key": "PMC8548620"}], "notes": [], "created": "2021-12-09T20:01:04.589Z", "modified": "2025-10-17T13:03:15.685Z"}], "created": "2021-12-09T20:01:04.615Z", "modified": "2021-12-09T20:01:04.615Z"}