ReviewCell death discovery2024
The roles of Th cells in myocardial infarction.
Review in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed.
- Optimized cardiac leukocyte isolation for flow cytometry enumeration and sorting.American journal of physiology. Heart and circulatory physiology · 2026Article
- Injury polarized CD4Redox biology · 2026Article
- Th1/Th17-Treg Imbalance in Asian Atrial Fibrillation: Subtype and Demographic Heterogeneity.JACC. Asia · 2026Article
- Diverse Roles of Semaphorins on T Cell Activation, Differentiation, Migration, and Effector Functions.Cells · 2026Review
- Cardioprotective effects of hesperidin-loaded biodegradable mesoporous copper to reduce cardiomyocyte apoptosis for myocardial infarction.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Research advances in intelligent microenvironment-responsive hydrogels for myocardial infarction therapy.APL bioengineering · 2026Review
- Article
- Spatial and Functional Immune Profiling Identifies Impaired Vascular Repair in Human Myocardial Infarction.Biomedicines · 2026Article
- Differences in heart DNA methylation between sudden infant death syndrome and other sudden deaths.Clinical epigenetics · 2026Article
- Integrative transcriptomic analysis identifies an oxidative stress-associated diagnostic signature for myocardial infarction.Journal of thrombosis and thrombolysis · 2026Article
- The spleen-brain axis in Alzheimer's disease and related dementias: Integrating immune and metabolic regulation.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Distinct immunometabolic signatures of type 1 versus type 2 diabetes in a murine model of myocardial infarction.Cardiovascular diabetology · 2026Article
- Targeting the Th17/Treg axis: from immunological insights to therapeutic avenues in atherosclerosis.Frontiers in immunology · 2026Review
- Stem cell-derived extracellular vesicles as immunomodulators: a novel paradigm for post-myocardial infarction repair and regeneration.Frontiers in pharmacology · 2026Review
- Article
- Immune Mechanisms in Myocardial Remodeling Following Myocardial Infarction: Focusing on Regulatory Networks of T Cell Responses.Journal of inflammation research · 2026Review
- Regional and cell specific bioactivity of injectable extracellular matrix biomaterials in myocardial infarction.Nature communications · 2025Article
- Ex vivo single-cell profiling of acute myocardial infarction patients reveals disproportionate CD66bBioengineering & translational medicine · 2025Article
- Association of Pan-Immune-Inflammation Value with All-Cause and Cardiovascular Mortality in Survivors of Myocardial Infarction: NHANES 2001-2018 Analysis.Journal of cardiovascular development and disease · 2025Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
Myocardial infarction, commonly known as a heart attack, is a serious condition caused by the abrupt stoppage of blood flow to a part of the heart, leading to tissue damage. A significant aspect of this condition is reperfusion injury, which occurs when blood flow is restored but exacerbates the damage. This review first addresses the role of the innate immune system, including neutrophils and macrophages, in the cascade of events leading to myocardial infarction and reperfusion injury. It then shifts focus to the critical involvement of CD4+ T helper cells in these processes. These cells, pivotal in regulating the immune response and tissue recovery, include various subpopulations such as Th1, Th2, Th9, Th17, and Th22, each playing a unique role in the pathophysiology of myocardial infarction and reperfusion injury. These subpopulations contribute to the injury process through diverse mechanisms, with cytokines such as IFN-γ and IL-4 influencing the balance between tissue repair and injury exacerbation. Understanding the interplay between the innate immune system and CD4+ T helper cells, along with their cytokines, is crucial for developing targeted therapies to mitigate myocardial infarction and reperfusion injury, ultimately improving outcomes for cardiac patients.
Identifiers
What OpenQuestion holds
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.