ArticleMolecular medicine (Cambridge, Mass.)
Aging influences cardiac mitochondrial gene expression and cardiovascular function following hemorrhage injury.
Article in Molecular medicine (Cambridge, Mass.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- CHIP and aging: a key regulator of proteostasis and cellular senescence.Biogerontology · 2025Review
- Plasma Extracellular Vesicle-Derived miR-296-5p is a Maturation-Dependent Rejuvenation Factor that Downregulates Inflammation and Improves Survival after Sepsis.Journal of extracellular vesicles · 2025Article
- Senescence landscape in the liver following sepsis and senolytics as potential therapeutics.Aging cell · 2025Article
- Au-modified ceria nanozyme prevents and treats hypoxia-induced pulmonary hypertension with greatly improved enzymatic activity and safety.Journal of nanobiotechnology · 2024Article
- Interactions of Cellular Energetic Gene Clusters in the Alzheimer's Mouse Brain.Molecular neurobiology · 2024Article
- Juvenile Plasma Factors Improve Organ Function and Survival following Injury by Promoting Antioxidant Response.Aging and disease · 2022Article
- Regulation of NADMetabolism: clinical and experimental · 2022Review
- Kaempferol Alleviates Oxidative Stress and Apoptosis Through Mitochondria-dependent Pathway During Lung Ischemia-Reperfusion Injury.Frontiers in pharmacology · 2021Article
- Pathological Responses of Cardiac Mitochondria to Burn Trauma.International journal of molecular sciences · 2020Review
- Metabolomics Coupled with Transcriptomics Approach Deciphering Age Relevance in Sepsis.Aging and disease · 2019Article
- Mitochondria and cardiovascular diseases-from pathophysiology to treatment.Annals of translational medicine · 2018Review
- The potential mechanism of mitochondrial dysfunction in septic cardiomyopathy.The Journal of international medical research · 2018Article
- Epigenetic Regulatory Mechanisms Induced by Resveratrol.Nutrients · 2017Review
- Mitochondrial function in hypoxic ischemic injury and influence of aging.Progress in neurobiology · 2017Review
- High-resolution profiles of gene expression and DNA methylation highlight mitochondrial modifications during early embryonic development.The Journal of reproduction and development · 2017Article
- Mitochondrial and Metabolic Gene Expression in the Aged Rat Heart.Frontiers in physiology · 2016Article
- Sexual dimorphism in the expression of mitochondria-related genes in rat heart at different ages.PloS one · 2015Article
- Aging and injury: alterations in cellular energetics and organ function.Aging and disease · 2014Review
- Resveratrol restores sirtuin 1 (SIRT1) activity and pyruvate dehydrogenase kinase 1 (PDK1) expression after hemorrhagic injury in a rat model.Molecular medicine (Cambridge, Mass.) · 2014Article
- Induction of neuronal mitophagy in acute spinal cord injury in rats.Neurotoxicity research · 2013Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Cardiac dysfunction and mortality associated with trauma and sepsis increase with age. Mitochondria play a critical role in the energy demand of cardiac muscles, and thereby on the function of the heart. Specific molecular pathways responsible for mitochondrial functional alterations after injury in relation to aging are largely unknown. To further investigate this, 6- and 22-month-old rats were subjected to trauma-hemorrhage (T-H) or sham operation and euthanized following resuscitation. Left ventricular tissue was profiled using our custom rodent mitochondrial gene chip (RoMitochip). Our experiments demonstrated a declined left ventricular performance and decreased alteration in mitochondrial gene expression with age following T-H and we have identified c-Myc, a pleotropic transcription factor, to be the most upregulated gene in 6- and 22-month-old rats after T-H. Following T-H, while 142 probe sets were altered significantly (39 up and 103 down) in 6-month-old rats, only 66 were altered (30 up and 36 down) in 22-month-old rats; 36 probe sets (11 up and 25 down) showed the same trend in both groups. The expression of c-Myc and cardiac death promoting gene Bnip3 were increased, and Pgc1-α and Ppar-α a decreased following T-H. Eleven tRNA transcripts on mtDNA were upregulated following T-H in the aged animals, compared with the sham group. Our observations suggest a c-myc-regulated mitochondrial dysfunction following T-H injury and marked decrease in age-dependent changes in the transcriptional profile of mitochondrial genes following T-H, possibly indicating cellular senescence. To our knowledge, this is the first report on mitochondrial gene expression profile following T-H in relation to aging.
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