ArticleCardiovascular research2014
The number of X chromosomes influences protection from cardiac ischaemia/reperfusion injury in mice: one X is better than two.
Article in Cardiovascular research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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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.
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Who cites it
67 citing papers in PubMed, 108 citations in OpenAlex.
- Macrophages and the Survival of Cardiomyocytes After Myocardial Infarction.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Histone Modifications in Cardiovascular Disease: Mechanisms and Therapeutic Opportunities.MedComm · 2026Review
- Sex-specific insights in atherosclerosis and pulmonary arterial hypertension: an overlooked comorbidity.Frontiers in cardiovascular medicine · 2026Review
- Escape of Kdm6a from X Chromosome Is Detrimental to Ischemic Brains via IRF5 Signaling.Translational stroke research · 2025Article
- Sex differences in pulmonary (arterial) hypertension: does it matter?Current opinion in pulmonary medicine · 2025Review
- Anti-ageing interventions for the treatment of cardiovascular disease.Cardiovascular research · 2025Review
- Hybrid molecule SA-10 and its PLGA nanosuspension protect human and rodent retinal ganglion cells against neuronal injury.BMC neuroscience · 2025Article
- Signals from the extracellular matrix: Region- and sex-specificity in cardiac aging.Current opinion in cell biology · 2025Review
- Current anti-inflammatory strategies for treatment of heart failure: From innate to adaptive immunity.Pharmacological research · 2025Review
- Sex Chromosomes and Sex Hormones: Dissecting the Forces That Differentiate Female and Male Hearts.Circulation · 2025Review
- Sex as a biological variable in ageing: insights and perspectives on the molecular and cellular hallmarks.Open biology · 2024Review
- Escape of Kdm6a from X chromosome is detrimental to ischemic brains via IRF5 signaling.Research square · 2024Article
- Sex Differences in Cardiovascular Diseases: Exploring the Role of Microbiota and Immunity.Biomedicines · 2024Review
- Hearts apart: sex differences in cardiac remodeling in health and disease.The Journal of clinical investigation · 2024Review
- Testosterone deficiency promotes arterial stiffening independent of sex chromosome complement.Biology of sex differences · 2024Article
- Article
- Gender-specific genetic and epigenetic signatures in cardiovascular disease.Frontiers in cardiovascular medicine · 2024Review
- Reporting Sex and Gender Differences in Cardiovascular Research.US cardiology · 2024Review
- Guidelines on the use of sex and gender in cardiovascular research.American journal of physiology. Heart and circulatory physiology · 2024Review
- Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
aimSex differences in coronary heart disease have been attributed to sex hormones, whereas the potential role of the sex chromosomes has been ignored so far. Here, we investigated the role of the sex chromosomes in causing sex differences in myocardial ischaemia/reperfusion (I/R) injury. METHODS AND
resultsWe used two unique mouse models, the 'four core genotypes' [XX mice with ovaries (XXF) or testes (XXM) and XY mice with ovaries (XYF) or testes (XYM)] and XY* (gonadal male or female mice with one or two X chromosomes). All mice were gonadectomized (GDX). In vivo or isolated Langendorff-perfused hearts were subjected to I/R injury. The in vivo infarct size in XY mice was significantly smaller than XX mice regardless of their gonadal type (24.5 ± 4.1% in XYF and 21.8 ± 3.3% in XYM vs. 37.0 ± 3.2% in XXF and 35.5 ± 2.1% in XXM, P < 0.01). Consistent with the results in vivo, the infarct size was markedly smaller and cardiac functional recovery was significantly better in XY mice compared with XX ex vivo. The mitochondrial calcium retention capacity was significantly higher in XY compared with XX mice (nmol/mg protein: XXF = 126 ± 9 and XXM = 192 ± 45 vs. XYF = 250 ± 56 and XYM = 286 ± 51, P < 0.05). In XY* mice, mice with 2X chromosomes had larger infarct size (2X females = 41.4 ± 8.9% and 2X males = 46.3 ± 9.5% vs. 1X females = 23.7 ± 3.9% and 1X males = 26.6 ± 6.9%, P < 0.05) and lower heart functional recovery, compared with those with 1X chromosome. Several X genes that escape X inactivation (Eif2s3x, Kdm6a, and Kdm5c) showed higher expression in XX than in XY hearts.
conclusionXX mice have higher vulnerability to I/R injury compared with XY mice, which is due to the number of X chromosomes rather than the absence of the Y chromosome.
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Registered trials
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