ReviewFrontiers in immunology2025
GSDME in cardiovascular diseases: research system and contemporary progress.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Phytomedicines modulate pyroptosis in cardiovascular diseases: pre-clinical evidence, limitations and translational perspectives.Frontiers in pharmacology · 2026Review
- Neutrophil extracellular traps and pyroptosis: a molecular nexus linking systemic autoimmune diseases to atherosclerosis.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite considerable advancements in treatment technologies in recent years, cardiovascular diseases still pose a significant threat to human health. Pyroptosis is a novel type of regulated cell death (RCD) associated with inflammation and innate immunity. Gasdermin E (GSDME), a key member of the gasdermin family, serves as a critical mediator of pyroptosis. Upon recognizing cellular stress or damage, GSDME can be activated through the classic caspase-3 cleavage pathway, releasing its N-terminal domain, which forms pores in the cell membrane to mediate pyroptosis and promote the release of inflammatory cytokines. Increasing evidence suggests that this process is closely associated with the progression of cardiovascular diseases, including atherosclerosis, myocardial infarction, nonischemic cardiomyopathy, and pulmonary arterial hypertension. These findings highlight the therapeutic potential of GSDME, with strategies targeting GSDME showing promising preclinical prospects. In this review, we introduce the structure and biological functions of GSDME, provide a brief overview of research strategies and experimental systems, and discuss recent scientific advances regarding GSDME in cardiovascular diseases. In addition, we explore the challenges currently facing the field and future research directions. A deeper understanding of the molecular mechanisms of GSDME in the cardiovascular system will provide a theoretical basis for the development of novel therapeutic strategies.
Indexed as
Identifiers
What Socratic 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 Socratic graph.