The human heart heals from injury through specific cellular regeneration and scarring mechanisms
the verdict
SUPPORTED
the evidence backs this
confidence 87/100
The human and mammalian heart responds to injury through a combination of limited cellular regeneration (such as cardiomyocyte cell-cycle re-entry or proliferation) and scarring/fibrosis mechanisms.
Evidence for · 7
Agrin promotes coordinated therapeutic processes leading to improved cardiac repair in pigs
2019 · cited by 87
Paper 0 demonstrates that interventions like Agrin can promote cell cycle re-entry and reduce fibrosis during cardiac repair.
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More for · 6
Tenascin-C in cardiac disease: A sophisticated controller of inflammation, repair, and fibrosis.
2020 · cited by 85
Paper 1 discusses Tenascin-C as a key extracellular matrix controller of tissue repair and fibrosis in the heart.
Cardiac cellular diversity and functionality in cardiac repair by single-cell transcriptomics
2023 · cited by 6
Paper 2 highlights how single-cell transcriptomics uncovers endogenous myocardial regeneration and myocardial fibrosis as core repair mechanisms.
Hydrogels loaded with different substances for treating heart failure: a promising therapy.
2026 · cited by 0
Paper 7 notes that excessive fibrosis and cardiomyocyte death characterize heart injury, which hydrogels attempt to address by promoting repair.
Cardiac regeneration and repair: the emerging mechanisms and therapeutic approaches.
2026 · cited by 0
Paper 8 details how promoting cardiomyocyte proliferation and managing extracellular matrix remodeling govern cardiac regeneration.
Extracellular Vesicles in Cardiac Repair Approaches: Implications for In Vitro Heart Models and Potential ATMP Development.
2026 · cited by 0
Paper 10 explains that the loss of functional cardiomyocytes and subsequent fibrotic scar formation characterize cardiac injury and repair processes.
Dimethyl fumarate attenuates post-infarct myocardial injury and is associated with modulation of the NRG-1/ErbB2/Akt pathway and reduction of oxidative stress.
2026 · cited by 0
Paper 11 shows that treatments can enhance cardiomyocyte proliferation and reduce cardiac fibrosis following myocardial infarction.