ArticleTranslational research : the journal of laboratory and clinical medicine2024
Chronic kidney disease and left ventricular diastolic dysfunction (CKD-LVDD) alter cardiac expression of mitochondria-related genes in swine.
Article in Translational research : the journal of laboratory and clinical medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 10 citations in OpenAlex.
- Renal single-nucleus transcriptomic of a new model of cardiovascular-kidney-metabolic syndrome in aging swine.American journal of physiology. Renal physiology · 2026Article
- Chronic kidney disease induces a distinct lipidomic signature and accelerates atherosclerosis progression in a novel minipig model.Laboratory animal research · 2026Article
- From kidney injury to cardiac dysfunction: the central role of oxidative stress in diabetes and CKD.Basic research in cardiology · 2026Article
- When in doubt, pig it out: a versatile translational platform to study CKD, HFpEF, and CKM syndrome.American journal of physiology. Heart and circulatory physiology · 2025Review
- Recharging the Powerhouse: Mitochondrial Dysfunction and Therapy in Cardiorenal Syndrome Type 4.Current heart failure reports · 2025Review
- Coronary microvascular disease in heart failure with preserved ejection fraction.Physiological reports · 2025Review
- Sexual dimorphism in animal models of heart failure with preserved ejection fraction.Journal of applied physiology (Bethesda, Md. : 1985) · 2025Review
- Renal ischemia alters the mRNA and miRNA profile of vasculature-related genes in scattered tubular-like cells from female pigs.American journal of physiology. Renal physiology · 2025Article
- A New Model of Chronic Kidney Disease, Metabolic Derangements, and Heart Failure with Preserved Ejection Fraction in Aging Swine.American journal of nephrology · 2025Article
- Oxidative stress initiates hemodynamic change in CKD-induced heart disease.Basic research in cardiology · 2024Article
- Vasodilator reactive oxygen species ameliorate perturbed myocardial oxygen delivery in exercising swine with multiple comorbidities.Basic research in cardiology · 2024Article
- Expanding landscape of coronary microvascular disease in co-morbid conditions: Metabolic disease and beyond.Journal of molecular and cellular cardiology · 2024Review
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Cardiovascular disease and heart failure doubles in patients with chronic kidney disease (CKD), but the underlying mechanisms remain obscure. Mitochondria are central to maintaining cellular respiration and modulating cardiomyocyte function. We took advantage of our novel swine model of CKD and left ventricular diastolic dysfunction (CKD-LVDD) to investigate the expression of mitochondria-related genes and potential mechanisms regulating their expression. CKD-LVDD and normal control pigs (n=6/group, 3 males/3 females) were studied for 14 weeks. Renal and cardiac hemodynamics were quantified by multidetector-CT, echocardiography, and pressure-volume loop studies, respectively. Mitochondrial morphology (electron microscopy) and function (Oroboros) were assessed ex vivo. In randomly selected pigs (n=3/group), cardiac mRNA-, MeDIP-, and miRNA-sequencing (seq) were performed to identify mitochondria-related genes and study their pre- and post -transcriptional regulation. CKD-LVDD exhibited cardiac mitochondrial structural abnormalities and elevated mitochondrial H2O2 emission but preserved mitochondrial function. Cardiac mRNA-seq identified 862 mitochondria-related genes, of which 69 were upregulated and 33 downregulated (fold-change ≥2, false discovery rate≤0.05). Functional analysis showed that upregulated genes were primarily implicated in processes associated with oxidative stress, whereas those downregulated mainly participated in respiration and ATP synthesis. Integrated mRNA/miRNA/MeDIP-seq analysis showed that upregulated genes were modulated predominantly by miRNAs, whereas those downregulated were by miRNA and epigenetic mechanisms. CKD-LVDD alters cardiac expression of mitochondria-related genes, associated with mitochondrial structural damage but preserved respiratory function, possibly reflecting intrinsic compensatory mechanisms. Our findings may guide the development of early interventions at stages of cardiac dysfunction in which mitochondrial injury could be prevented, and the development of LVDD ameliorated.
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