Summary
This narrative review synthesises evidence on intracellular signalling pathways central to myocardial infarction pathophysiology, spanning inflammation, oxidative stress, apoptosis, fibrosis, and angiogenesis. The authors evaluate emerging therapeutic modalities—including drug, gene, protein, cell, and exosome therapies—designed to modulate these pathways and promote cardiac repair and functional recovery following ischaemic injury.
UK applicability
As a mechanistic review of cellular signalling and experimental therapeutic approaches, findings are relevant to UK cardiac research and drug development pipelines, though clinical translation and health-economic applicability would require evidence from UK or comparable healthcare systems.
Key measures
Signalling pathway involvement in cardiomyocyte survival, proliferation, apoptosis, and autophagy; inflammation markers (NLRP3/caspase-1, TLR4/MyD88/NF-κB); oxidative stress and apoptosis mediators (Notch, Hippo/YAP, RhoA/ROCK, Nrf2/HO-1); myocardial fibrosis controllers (TGF-β/SMADs, Wnt/β-catenin); angiogenesis regulators (PI3K/Akt, MAPK, JAK/STAT)
Outcomes reported
The review synthesises evidence on cell signalling pathways implicated in myocardial infarction pathology across multiple cell types, and evaluates emerging therapeutic strategies (drug, gene, protein, cell, and exosome therapies) targeting these pathways to inhibit cardiomyocyte death, reduce inflammation, and enhance angiogenesis.
Topic tags
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