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Pyroptosis is an inflammatory form of programmed cell death (PCD), driven by the activation of inflammasomes and inflammatory caspases. These molecular events trigger the proteolytic cleavage of gasdermin proteins, leading to membrane pores formation, cell lysis, and the subsequent release of cellular contents. Induction of pyroptosis amplifies inflammation, contributing to severe inflammatory responses and accelerating the pathogenesis of various chronic inflammation-related diseases. Myocardial fibrosis (MF) is characterized by the deposition of scar tissue in the heart, stemming from an aberrant wound healing response to inflammatory damage. It is a prevalent pathological feature in a range of cardiovascular diseases. Given the complex nature of wound repair and fibrosis following myocardial injury, treatments that target only specific contributors to disease pathogenesis show limited efficacy in mitigating fibrosis. While significant progress has been made in understanding the mechanisms underlying pyroptosis, its regulatory processes in MF remain incompletely understood, and strategies to improve clinical outcomes are still lacking. This review provides an in-depth examination of the latest insights into the regulatory mechanisms of pyroptosis, newly identified influencing factors, and its role in myocardial inflammation and fibrosis. Additionally, we discuss potential anti-fibrotic therapies targeting pyroptosis for the management of MF, highlighting challenges and future directions in this field.