ReviewNature reviews. Cardiology2024
The role of cardiac pericytes in health and disease: therapeutic targets for myocardial infarction.
Review in Nature reviews. Cardiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- Reprogramming heart failure: physiological orchestration and mechanistic decoding of exercise benefits.BMC cardiovascular disorders · 2025Pooled it
- Cardiac-targeted delivery of miRNA via antioxidant nanozymes ameliorates cardiac dysfunction and fibrosis after myocardial infarction.Journal of nanobiotechnology · 2026Article
- Infusible Extracellular Matrix Biomaterial Enhances Cell-Specific Pro-Repair Responses Following Acute Myocardial Infarction.Advanced healthcare materials · 2026Article
- Proteolytic remodelling of the extracellular matrix by pericytes.The FEBS journal · 2026Review
- Molecular damage associated with ageing drives inflammation in cardiovascular disease.Nature reviews. Cardiology · 2026Review
- Cardioprotective effects of hesperidin-loaded biodegradable mesoporous copper to reduce cardiomyocyte apoptosis for myocardial infarction.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- RelJournal of translational medicine · 2026Article
- Single-cell polygenic risk scores dissect cellular and molecular heterogeneity of complex human diseases.Nature biotechnology · 2026Article
- Linking Heat Stress to Impaired Cardiac Repair: The ER Stress-Angiogenesis Axis as a Critical Barrier.International journal of molecular sciences · 2026Review
- ILC2-derived IL-9 activates regulatory T cells to facilitate post-myocardial infarction repair.Cell communication and signaling : CCS · 2026Article
- uPAR deficiency triggers TGFβ1-mediated fibrotic remodeling in a cardiac perivascular-like microenvironment.Stem cell research & therapy · 2026Article
- Leveraging Single-Cell Technologies to Advance Understanding of Myocardial Disease.Circulation research · 2026Review
- The role of the bidirectional regulatory network between immune cells and stromal cells in cardiac repair and fibrosis following myocardial infarction.Frontiers in immunology · 2026Review
- Profibrotic macrophage-derived CXCL4 promotes pericyte-to-myofibroblast transition after spinal cord injury.Journal of orthopaedic translation · 2026Article
- Spatiotemporal Atlas of Heart Development Reveals Blood-Flow-Dependent Cellular, Structural, Metabolic, and Spatial Remodeling.bioRxiv : the preprint server for biology · 2025Article
- Integrative single-cell and spatial transcriptome analysis reveals the functions of TREM2Molecular and cellular biochemistry · 2025Article
- Article
- Early pathological changes of coronary microvasculation in heart failure with preserved ejection fraction.BMC cardiovascular disorders · 2025Article
- Infusible Extracellular Matrix Biomaterial Enhances Cell-Specific Pro-Repair Responses Following Acute Myocardial Infarction.bioRxiv : the preprint server for biology · 2025Article
- PRRX1 Orchestrates Pericyte-Myofibroblast Transition in Pathological Retinal Fibrosis.Investigative ophthalmology & visual science · 2025Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Millions of cardiomyocytes die immediately after myocardial infarction, regardless of whether the culprit coronary artery undergoes prompt revascularization. Residual ischaemia in the peri-infarct border zone causes further cardiomyocyte damage, resulting in a progressive decline in contractile function. To date, no treatment has succeeded in increasing the vascularization of the infarcted heart. In the past decade, new approaches that can target the heart's highly plastic perivascular niche have been proposed. The perivascular environment is populated by mesenchymal progenitor cells, fibroblasts, myofibroblasts and pericytes, which can together mount a healing response to the ischaemic damage. In the infarcted heart, pericytes have crucial roles in angiogenesis, scar formation and stabilization, and control of the inflammatory response. Persistent ischaemia and accrual of age-related risk factors can lead to pericyte depletion and dysfunction. In this Review, we describe the phenotypic changes that characterize the response of cardiac pericytes to ischaemia and the potential of pericyte-based therapy for restoring the perivascular niche after myocardial infarction. Pericyte-related therapies that can salvage the area at risk of an ischaemic injury include exogenously administered pericytes, pericyte-derived exosomes, pericyte-engineered biomaterials, and pharmacological approaches that can stimulate the differentiation of constitutively resident pericytes towards an arteriogenic phenotype. Promising preclinical results from in vitro and in vivo studies indicate that pericytes have crucial roles in the treatment of coronary artery disease and the prevention of post-ischaemic heart failure.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.