ArticleMolecular medicine reports2020
Dexmedetomidine alleviated sepsis‑induced myocardial ferroptosis and septic heart injury.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers, 1 of them a synthesis that pooled it.
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
155 citing papers in PubMed, 1 synthesis or guideline pooled it, 233 citations in OpenAlex.
- Mapping current research and identifying hotspots of ferroptosis in cardiovascular diseases.Frontiers in cardiovascular medicine · 2022Pooled it
- Effect of superficial cervical plexus nerve block with Ropivacaine or a combination of different adjuvants on perioperative analgesia and quality of postoperative recovery in patients undergoing radical thyroid cancer surgery under general anesthesia: a prospective randomized controlled trial.World journal of surgical oncology · 2025Trial
- Effect of preoperative dexmedetomidine administration on the bispectral index in children during sevoflurane inhalation anesthesia: a randomized controlled trial.BMC anesthesiology · 2025Trial
- Cuproptosis in Ischemic Stroke: Molecular Mechanisms and Therapeutic Potential.Molecules (Basel, Switzerland) · 2026Review
- Ferroptosis as a target mechanism in heart and kidney disease.The Journal of clinical investigation · 2026Review
- Deltex E3 ubiquitin ligase 2 prevents sepsis-induced myocardial injury through degrading TfR1 via promoting K27-linked ubiquitination.Cell death and differentiation · 2026Article
- Molecular mechanisms of iron metabolism and ferroptosis in cardiovascular diseases and intervention strategies targeting natural products (Review).Molecular medicine reports · 2026Review
- Ferroptosis-related TFRC: a potential therapeutic target in sepsis and regulatory effect of γ-Tocotrienol.Human genomics · 2026Article
- Retrospective Evaluation of Anesthetic-Analgesic Protocols in Cats with and Without Transient Myocardial Thickening Following Gonadectomy.Animals : an open access journal from MDPI · 2026Article
- Protective Effects of Dexmedetomidine Against Ischemic Heart Disease and Diabetic Cardiomyopathy by Targeting Ferroptosis.Reviews in cardiovascular medicine · 2026Review
- Research Progress on the Role of Traditional Chinese Medicine in Regulating Ferroptosis in Cardiovascular Diseases.Biology · 2026Review
- Inhibition of iron overload and ferroptosis attenuates sepsis-induced myocardial injury in mice through STAT3/Lcn2 pathway.Journal of cardiothoracic surgery · 2026Article
- Dexmedetomidine improves sleep quality and alleviates emotional dysfunction by attenuating α-synuclein deposition in mice with sepsis-associated encephalopathy.Journal of advanced research · 2026Article
- The interactions of copper, glutamate, and cuproptosis: insights into brain health and Alzheimer's disease pathology.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Review
- A Phycoerythrin-SOD Fluorescent Probe Enables Detection of Oxidative Stress for Assessing Astaxanthin in NAFLD.Antioxidants (Basel, Switzerland) · 2026Article
- Non-apoptotic Regulated Cell Death Mechanisms in Sepsis and their Therapeutic Potential.Inflammation · 2026Review
- Dexmedetomidine Inhibits Ferroptosis to Alleviate Hypoxia/Reoxygenation-Induced Cardiomyocyte Injury by Regulating the HDAC2/FPN Pathway.Cardiovascular drugs and therapy · 2026Article
- The Regulatory Landscape of Ferroptosis and Iron Homeostasis: Pathophysiological Mechanisms and Therapeutic Horizons in Cardiovascular Disease.Drug design, development and therapy · 2026Review
- Ferroptosis suppressor protein 1-mediated ferroptosis suppression in sepsis: non-canonical antioxidant pathways, inflammatory regulation, and therapeutic perspectives.Frontiers in immunology · 2026Review
- Targeting ferroptosis in sepsis-induced cardiomyopathy: mechanisms and therapeutic potential of traditional Chinese Medicine.Frontiers in pharmacology · 2026Review
95 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac dysfunction resulting from sepsis may cause significant morbidity and mortality, and ferroptosis plays a role in this pathology. Dexmedetomidine (Dex), a α2‑adrenergic receptor (α2‑AR) agonist exerts cardioprotective effects against septic heart dysfunction, but the exact mechanism is unknown. In the present study, sepsis was induced by cecal ligation and puncture (CLP) in male C57BL/6 mice. Dex and yohimbine hydrochloride (YOH), an α2‑AR inhibitor, were administered before inducing CLP. Then, 24 h after CLP, serum and heart tissue were collected to detect changes of troponin‑I (TN‑I), interleukin 6 (IL‑6), superoxide dismutase (SOD), malonaldehyde (MDA) and glutathione (GSH) levels, and iron release. Ferroptosis‑targeting proteins, apoptosis and inflammatory factors were assessed by western blotting or ELISA. It was found that, 24 h after CLP, TN‑I, a biomarker of myocardial injury, was significantly increased compared with the control group. Furthermore, the levels of MDA, 8‑hydroxy‑2'‑deoxyguanosine and the inflammatory factors IL‑6 and monocyte chemoattractant protein‑1 were also significantly increased. It was demonstrated that treatment with Dex reverted or attenuated these changes (CLP + Dex vs. CLP; P<0.05), but these protective effects of Dex were reversed by YOH. Moreover, CLP significantly decreased the protein expression levels of glutathione peroxidase 4 (GPX4), SOD and GSH. However, CLP increased expression levels of heme oxygenase‑1 (HO‑1), transferrin receptor, cleaved caspase 3, inducible nitric oxide synthase and gasdermin D, and iron concentrations. It was found that Dex reversed these changes, but YOH abrogated the protective effects of Dex (CLP + Dex + YOH vs. CLP + Dex; P<0.05). Therefore, the present results suggested that the attenuation of sepsis‑induced HO‑1 overexpression and iron concentration, and the reduction of ferroptosis via enhancing GPX4, may be the major mechanisms via which Dex alleviates sepsis‑induced myocardial cellular injury.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.