ReviewInternational journal of molecular sciences2025
Mitochondria, Sex, and Cardiovascular Disease: A Complex Interplay.
Review in International journal of molecular sciences, 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.
- Tricarboxylic acid cycle metabolite index predicts adverse outcomes in acute myocardial infarction patients.BMC medicine · 2026Article
- Direct exposure to vinclozolin induces sex-dependent mitochondrial dysfunction in mouse liver.Current research in toxicology · 2026Article
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
Abstract
Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality worldwide. Increasing evidence indicates that sex differences significantly influence the development, progression, and outcomes of CVDs. Recent advances have highlighted the central role of mitochondria, not only as cellular energy hubs but also as key regulators of oxidative stress, inflammation, and apoptosis, in mediating sex-specific cardiovascular responses. This review explores sexual dimorphism in cardiovascular disease, focusing on the interplay between mitochondrial function and sex hormones in cardiovascular tissues. We summarize current evidence on the molecular, hormonal, and cellular mechanisms contributing to sex-based disparities in cardiovascular outcomes. Preclinical studies suggest that female cardiac mitochondria may exhibit greater antioxidant capacity and produce fewer reactive oxygen species than male mitochondria, contributing to enhanced cardioprotection. Estrogen has been shown to influence mitochondrial bioenergetics and gene expression, affecting vascular tone, inflammation, and cardiac remodelling, whereas the role of testosterone remains less well defined. Additionally, sex-specific mitochondrial signalling responses have been reported under cardiac stress conditions, which may underlie differences in disease presentation and progression. A better understanding of how sex modulates mitochondrial function could improve risk stratification and support the development of personalized prevention and treatment strategies. Further research is needed to translate these mechanistic insights into clinical practice.
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.