ArticleRedox biology2018
Identification of homocysteine-suppressive mitochondrial ETC complex genes and tissue expression profile - Novel hypothesis establishment.
Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 36 citations in OpenAlex.
- Effects of Vitamin B6 and Folic Acid on Cardiometabolic Biomarkers and Cardiac Oxidative Stress in Homocysteine-Loaded Rats.Biomedicines · 2026Article
- Integrated proteomics and metabolomics reveal phytosesquiterpene lactones inhibit TNBC cell activity by depleting ATP synthesis and reprogramming primary metabolism.Scientific reports · 2026Article
- MTHFR variant links homocysteine metabolism and endothelial cell dysfunction by targeting mitophagy in human thoracic aortic dissection patient induced pluripotent stem cell (iPSC) models.Journal of advanced research · 2025Article
- Homocysteine interferes with Ndufa1 leading to mitochondrial dysfunction through repression of the NADCell death & disease · 2025Article
- Mitochondrial complex-1 as a therapeutic target for cardiac diseases.Molecular and cellular biochemistry · 2025Review
- Metabolic landscape in venous thrombosis: insights into molecular biology and therapeutic implications.Annals of medicine · 2024Review
- Hyperhomocysteinemia-Induced Alterations in Protein Expression and Oxidative Stress Parameters in Rat Heart.Physiological research · 2024Article
- Focus on Mitochondrial Respiratory Chain: Potential Therapeutic Target for Chronic Renal Failure.International journal of molecular sciences · 2024Review
- Individual and joint effects of borderline ankle-brachial index and high plasma total homocysteine on all-cause death in hypertensive adults.Journal of geriatric cardiology : JGC · 2022Article
- Association Between Hyperhomocysteinemia Combined with Metabolic Syndrome and Higher Prevalence of Stroke in Chinese Adults Who Have Elevated Blood Pressure.Medical science monitor : international medical journal of experimental and clinical research · 2022Article
- Hyperhomocysteinemia exacerbates acute kidney injuryFrontiers in physiology · 2022Article
- Quantitative Crotonylome Analysis Reveals the Mechanism of Shenkang Injection on Diabetic Nephropathy.Oxidative medicine and cellular longevity · 2022Article
- Folic acid-induced animal model of kidney disease.Animal models and experimental medicine · 2021Review
- Molecular processes mediating hyperhomocysteinemia-induced metabolic reprogramming, redox regulation and growth inhibition in endothelial cells.Redox biology · 2021Article
- Relationship Between Plasma Total Homocysteine Levels and Mean Corrected TIMI Frame Count in Patients with Acute Myocardial Infarction.International journal of general medicine · 2021Article
- Homocysteine and Mitochondria in Cardiovascular and Cerebrovascular Systems.International journal of molecular sciences · 2020Review
- ROS systems are a new integrated network for sensing homeostasis and alarming stresses in organelle metabolic processes.Redox biology · 2020Review
- Homocysteine-methionine cycle is a metabolic sensor system controlling methylation-regulated pathological signaling.Redox biology · 2020Article
- Redox Regulation and Oxidative Stress: The Particular Case of the Stallion Spermatozoa.Antioxidants (Basel, Switzerland) · 2019Review
- Aberrant MFN2 transcription facilitates homocysteine-induced VSMCs proliferation via the increased binding of c-Myc to DNMT1 in atherosclerosis.Journal of cellular and molecular medicine · 2019Article
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Hyperhomocysteinemia (HHcy) is an independent risk factor for cardiovascular disease (CVD) which has been implicated in matochondrial (Mt) function impairment. In this study, we characterized Hcy metabolism in mouse tissues by using LC-ESI-MS/MS analysis, established tissue expression profiles for 84 nuclear-encoded Mt electron transport chain complex (nMt-ETC-Com) genes in 20 human and 19 mouse tissues by database mining, and modeled the effect of HHcy on Mt-ETC function. Hcy levels were high in mouse kidney/lung/spleen/liver (24-14 nmol/g tissue) but low in brain/heart (~5 nmol/g). S-adenosylhomocysteine (SAH) levels were high in the liver/kidney (59-33 nmol/g), moderate in lung/heart/brain (7-4 nmol/g) and low in spleen (1 nmol/g). S-adenosylmethionine (SAM) was comparable in all tissues (42-18 nmol/g). SAM/SAH ratio was as high as 25.6 in the spleen but much lower in the heart/lung/brain/kidney/liver (7-0.6). The nMt-ETC-Com genes were highly expressed in muscle/pituitary gland/heart/BM in humans and in lymph node/heart/pancreas/brain in mice. We identified 15 Hcy-suppressive nMt-ETC-Com genes whose mRNA levels were negatively correlated with tissue Hcy levels, including 11 complex-I, one complex-IV and two complex-V genes. Among the 11 Hcy-suppressive complex-I genes, 4 are complex-I core subunits. Based on the pattern of tissue expression of these genes, we classified tissues into three tiers (high/mid/low-Hcy responsive), and defined heart/eye/pancreas/brain/kidney/liver/testis/embryonic tissues as tier 1 (high-Hcy responsive) tissues in both human and mice. Furthermore, through extensive literature mining, we found that most of the Hcy-suppressive nMt-ETC-Com genes were suppressed in HHcy conditions and related with Mt complex assembly/activity impairment in human disease and experimental models. We hypothesize that HHcy inhibits Mt complex I gene expression leading to Mt dysfunction.
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