d688d1d3fc8dfa96f1a3eb29740844d1 308077.pdf 562e9e2e07644e8809dfd93c319f30e9a61615f3 308077.pdf 8ee7f35da10e7a4f59e3eeaa14a5c4a10cc9226e6462d3fd9d60fd3fa6c4ae51 308077.pdf Title: The Influence of Metabolic Risk Factors on the Inflammatory Response Triggered by Myocardial Infarction: Bridging Pathophysiology to Treatment Subject: Myocardial infarction (MI) sets off a complex inflammatory cascade that is crucial for effective cardiac healing and scar formation. Yet, if this response becomes excessive or uncontrolled, it can lead to cardiovascular complications. This review aims to provide a comprehensive overview of the tightly regulated local inflammatory response triggered in the early post-MI phase involving cardiomyocytes, (myo)fibroblasts, endothelial cells, and infiltrating immune cells. Next, we explore how the bone marrow and extramedullary hematopoiesis (such as in the spleen) contribute to sustaining immune cell supply at a cardiac level. Lastly, we discuss recent findings on how metabolic cardiovascular risk factors, including hypercholesterolemia, hypertriglyceridemia, diabetes, and hypertension, disrupt this immunological response and explore the potential modulatory effects of lifestyle habits and pharmacological interventions. Understanding how different metabolic risk factors influence the inflammatory response triggered by MI and unraveling the underlying molecular and cellular mechanisms may pave the way for developing personalized therapeutic approaches based on the patient’s metabolic profile. Similarly, delving deeper into the impact of lifestyle modifications on the inflammatory response post-MI is crucial. These insights may enable the adoption of more effective strategies to manage post-MI inflammation and improve cardiovascular health outcomes in a holistic manner. Keywords: myocardial infarction; inflammatory response; innate immune response; bone marrow; spleen; metabolic risk factors; lifestyle modifications; pharmacological interventions Author: Lisaidy Ramos-Regalado, Sebastià Alcover, Lina Badimon and Gemma Vilahur Creator: LaTeX with hyperref Producer: pdfTeX-1.40.25 CreationDate: Sat Jun 29 10:12:42 2024 CEST ModDate: Sat Jun 29 10:21:03 2024 CEST Custom Metadata: no Metadata Stream: no Tagged: no UserProperties: no Suspects: no Form: none JavaScript: no Pages: 18 Encrypted: no Page size: 595.276 x 841.89 pts (A4) Page rot: 0 File size: 2824609 bytes Optimized: no PDF version: 1.7 name type encoding emb sub uni object ID ------------------------------------ ----------------- ---------------- --- --- --- --------- WNWTFR+VnURWPalladioL-Bold Type 1 Custom yes yes yes 10 0 GCRDQP+URWPalladioL-Bold Type 1 Custom yes yes yes 16 0 NKRIJC+URWPalladioL-Roma Type 1 Custom yes yes yes 22 0 IQXMRV+URWPalladioL-Ital Type 1 Custom yes yes yes 27 0 CIEYAN+VnURWPalladioL Type 1 Custom yes yes yes 32 0 PFKOHU+TimesNewRomanPS-BoldItalicMT Type 1C WinAnsi yes yes no 48 0 GMZVMT+EURM10 Type 1 Builtin yes yes yes 65 0 ONBBOL+PalatinoLinotype,Bold TrueType WinAnsi yes yes no 80 0 ONBBOM+PalatinoLinotype CID TrueType Identity-H yes yes yes 83 0 ONBBPN+PalatinoLinotype TrueType WinAnsi yes yes no 89 0 ONBBPP+PalatinoLinotype,Italic TrueType WinAnsi yes yes no 92 0 ONBCCP+PalatinoLinotype,Bold TrueType MacRoman yes yes no 95 0 ONBCDA+PalatinoLinotype TrueType MacRoman yes yes no 98 0 ONBBOL+PalatinoLinotype,Bold TrueType WinAnsi yes yes no 113 0 ONBBOM+PalatinoLinotype CID TrueType Identity-H yes yes yes 116 0 ONBBPN+PalatinoLinotype TrueType WinAnsi yes yes no 122 0 ONBBPP+PalatinoLinotype,Italic TrueType WinAnsi yes yes no 125 0 ONBCDA+PalatinoLinotype TrueType MacRoman yes yes no 128 0 FXXUVH+CMSY10 Type 1 Builtin yes yes yes 139 0 ONBBOL+PalatinoLinotype,Bold TrueType WinAnsi yes yes no 154 0 ONBBOM+PalatinoLinotype CID TrueType Identity-H yes yes yes 157 0 ONBBPN+PalatinoLinotype TrueType WinAnsi yes yes no 163 0 ONBBPP+PalatinoLinotype,Italic TrueType WinAnsi yes yes no 166 0 ONBCDA+PalatinoLinotype TrueType MacRoman yes yes no 169 0 Jhove (Rel. 1.28.0, 2023-05-18) Date: 2025-02-25 02:45:40 CET RepresentationInformation: 308077.pdf ReportingModule: PDF-hul, Rel. 1.12.4 (2023-03-16) LastModified: 2025-02-24 11:46:25 CET Size: 2824609 Format: PDF Version: 1.7 Status: Well-Formed and valid SignatureMatches: PDF-hul MIMEtype: application/pdf PDFMetadata: Objects: 636 FreeObjects: 1 IncrementalUpdates: 0 DocumentCatalog: PageLayout: SinglePage PageMode: UseNone Outlines: Item: Title: Introduction Destination: section.1 Item: Title: Local Inflammatory Response Triggered by Myocardial Infarction Destination: section.2 Item: Title: The Involvement of the Bone Marrow and Spleen in the Systemic Inflammatory Response following Myocardial Infarction Destination: section.3 Item: Title: The Migration and Recruitment of Immune Cells to the Infarcted Heart Destination: section.4 Children: Item: Title: Neutrophils Destination: subsection.4.1 Item: Title: Monocyte/Macrophages Destination: subsection.4.2 Item: Title: Dendritic Cells Destination: subsection.4.3 Item: Title: Lymphocytes Destination: subsection.4.4 Item: Title: The Impact of Metabolic Cardiovascular Risk Factors on the Myocardial Infarction-Induced Inflammatory Response Destination: section.5 Item: Title: Impact of Lifestyle Changes and Therapeutic Approaches Destination: section.6 Item: Title: Conclusions and Future Perspectives Destination: section.7 Item: Title: References Destination: section.8 Info: Title: The Influence of Metabolic Risk Factors on the Inflammatory Response Triggered by Myocardial Infarction: Bridging Pathophysiology to Treatment Author: Lisaidy Ramos-Regalado, Sebastià Alcover, Lina Badimon and Gemma Vilahur Subject: Myocardial infarction (MI) sets off a complex inflammatory cascade that is crucial for effective cardiac healing and scar formation. Yet, if this response becomes excessive or uncontrolled, it can lead to cardiovascular complications. This review aims to provide a comprehensive overview of the tightly regulated local inflammatory response triggered in the early post-MI phase involving cardiomyocytes, (myo)fibroblasts, endothelial cells, and infiltrating immune cells. Next, we explore how the bone marrow and extramedullary hematopoiesis (such as in the spleen) contribute to sustaining immune cell supply at a cardiac level. Lastly, we discuss recent findings on how metabolic cardiovascular risk factors, including hypercholesterolemia, hypertriglyceridemia, diabetes, and hypertension, disrupt this immunological response and explore the potential modulatory effects of lifestyle habits and pharmacological interventions. Understanding how different metabolic risk factors influence the inflammatory response triggered by MI and unraveling the underlying molecular and cellular mechanisms may pave the way for developing personalized therapeutic approaches based on the patient’s metabolic profile. Similarly, delving deeper into the impact of lifestyle modifications on the inflammatory response post-MI is crucial. These insights may enable the adoption of more effective strategies to manage post-MI inflammation and improve cardiovascular health outcomes in a holistic manner. 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Subtype: Link Rect: 267, 339, 304, 349 Annotation: Subtype: Link Rect: 109, 305, 146, 315 Annotation: Subtype: Link Rect: 279, 270, 316, 280 Annotation: Subtype: Link Rect: 323, 270, 359, 280 Checksum: 5f7077db Type: CRC32 Checksum: d688d1d3fc8dfa96f1a3eb29740844d1 Type: MD5 Checksum: 562e9e2e07644e8809dfd93c319f30e9a61615f3 Type: SHA-1 Checksum: 8ee7f35da10e7a4f59e3eeaa14a5c4a10cc9226e6462d3fd9d60fd3fa6c4ae51 Type: SHA-256