ReviewFrontiers in cardiovascular medicine2021
Engineering the Cellular Microenvironment of Post-infarct Myocardium on a Chip.
Review in Frontiers in cardiovascular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
14 citing papers in PubMed, 26 citations in OpenAlex.
- Heart-on-a-chip and vasculature-on-a-chip platforms as models of cardiovascular disease.Nature reviews. Cardiology · 2026Review
- Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Review
- The role of cellular senescence-related genes in ischemia-reperfusion injury and the identification of their biomarkers.Scientific reports · 2026Article
- Substrate Stiffness Modulates Fibroblast Extracellular Vesicle Secretion Via Mechanotransduction Pathways.Small (Weinheim an der Bergstrasse, Germany) · 2025Article
- The future of cardiac repair: a review on cell-free nanotherapies for regenerative myocardial infarction.Drug delivery and translational research · 2025Review
- Cardiomyocytes in Hypoxia: Cellular Responses and Implications for Cell-Based Cardiac Regenerative Therapies.Bioengineering (Basel, Switzerland) · 2025Review
- Hypoxic-Normoxic Crosstalk Activates Pro-Inflammatory Signaling in Human Cardiac Fibroblasts and Myocytes in a Post-Infarct Myocardium on a Chip.Advanced healthcare materials · 2024Article
- Advancing Human iPSC-Derived Cardiomyocyte Hypoxia Resistance for Cardiac Regenerative Therapies through a Systematic Assessment of In Vitro Conditioning.International journal of molecular sciences · 2024Article
- 3D bioprinted aged human post-infarct myocardium tissue model.Health science reports · 2024Article
- Rebuilding the myocardial microenvironment to enhance mesenchymal stem cells-mediated regeneration in ischemic heart disease.Frontiers in bioengineering and biotechnology · 2024Review
- Regulation of cardiac fibroblasts by lymphocytes after a myocardial infarction: playing in the major league.American journal of physiology. Heart and circulatory physiology · 2023Review
- Tropoelastin Improves Post-Infarct Cardiac Function.Circulation research · 2023Article
- Integrated whole-genome gene expression analysis reveals an atlas of dynamic immune landscapes after myocardial infarction.Frontiers in cardiovascular medicine · 2023Article
- Myocardial infarction from a tissue engineering and regenerative medicine point of view: A comprehensive review on models and treatments.Biophysics reviews · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Myocardial infarctions are one of the most common forms of cardiac injury and death worldwide. Infarctions cause immediate necrosis in a localized region of the myocardium, which is followed by a repair process with inflammatory, proliferative, and maturation phases. This repair process culminates in the formation of scar tissue, which often leads to heart failure in the months or years after the initial injury. In each reparative phase, the infarct microenvironment is characterized by distinct biochemical, physical, and mechanical features, such as inflammatory cytokine production, localized hypoxia, and tissue stiffening, which likely each contribute to physiological and pathological tissue remodeling by mechanisms that are incompletely understood. Traditionally, simplified two-dimensional cell culture systems or animal models have been implemented to elucidate basic pathophysiological mechanisms or predict drug responses following myocardial infarction. However, these conventional approaches offer limited spatiotemporal control over relevant features of the post-infarct cellular microenvironment. To address these gaps, Organ on a Chip models of post-infarct myocardium have recently emerged as new paradigms for dissecting the highly complex, heterogeneous, and dynamic post-infarct microenvironment. In this review, we describe recent Organ on a Chip models of post-infarct myocardium, including their limitations and future opportunities in disease modeling and drug screening.
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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 Socratic graph.