ArticleMolecules (Basel, Switzerland)2018
Melatonin Balance the Autophagy and Apoptosis by Regulating UCP2 in the LPS-Induced Cardiomyopathy.
Article in Molecules (Basel, Switzerland), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
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Who cites it
41 citing papers in PubMed, 82 citations in OpenAlex.
- Melatonin Targets Mitochondrial Redox Homeostasis: Optimizing the Intracellular Microenvironment.International journal of molecular sciences · 2026Review
- Mitochondrial regulation of lactylation in sepsis-induced cardiomyopathy.Critical care (London, England) · 2025Review
- Advances in mitochondria-nucleus crosstalk in septic cardiomyopathy.Cell biology and toxicology · 2025Review
- The Protective Effect of Melatonin on LPS-Induced Myocardial InjuryCombinatorial chemistry & high throughput screening · 2025Article
- Article
- Curcumin pretreatment attenuates myocardial ischemia/reperfusion injury by inhibiting ferroptosis, autophagy and apoptosis via HES1.International journal of molecular medicine · 2024Article
- Group 2 innate lymphocytes protect the balance between autophagy and apoptosis in cardiomyocytes during sepsis-induced cardiac injury.Scientific reports · 2024Article
- Acute exposure to LPS induces cardiac dysfunction via the activation of the NLRP3 inflammasome.Scientific reports · 2024Article
- Chronobiotic and cytoprotective activity of melatonin in the cardiovascular system. Doses matter.Npj biological timing and sleep · 2024Review
- SIRT3 and RORα are two prospective targets against mitophagy during simulated ischemia/reperfusion injury in H9c2 cells.Heliyon · 2024Article
- Therapeutic Strategies Targeting Mitochondrial Dysfunction in Sepsis-induced Cardiomyopathy.Cardiovascular drugs and therapy · 2024Review
- The role of mitochondrial dynamics in disease.MedComm · 2023Review
- Inflammatory mechanisms and intervention strategies for sepsis-induced myocardial dysfunction.Immunity, inflammation and disease · 2023Review
- Propofol reduces lipopolysaccharide‑induced cardiomyocyte injury in sepsis by activating SIRT1‑mediated autophagy.Experimental and therapeutic medicine · 2023Article
- The potential influence of melatonin on mitochondrial quality control: a review.Frontiers in pharmacology · 2023Review
- Dynamic Plasma Lipidomic Analysis Revealed Cholesterol Ester and Amides Associated with Sepsis Development in Critically Ill Patients after Cardiovascular Surgery with Cardiopulmonary Bypass.Journal of personalized medicine · 2022Article
- Mechanisms and clinical evidence to support melatonin's use in severe COVID-19 patients to lower mortality.Life sciences · 2022Review
- Increase of Oxidative Stress by Deficiency of The ALDH2/UCP2/Nrf2 Axis Exacerbates Cardiac Dysfunction in Chronic Kidney Disease.Reviews in cardiovascular medicine · 2022Article
- Identification of novel biomarkers in septic cardiomyopathyFrontiers in genetics · 2022Article
- An Overview on Mitochondrial-Based Therapies in Sepsis-Related Myocardial Dysfunction: Mitochondrial Transplantation as a Promising Approach.The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2022Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To explore the mechanism of mitochondrial uncoupling protein 2 (UCP2) mediating the protective of melatonin when septic cardiomyopathy. UCP2 knocked out mice and cardiomyocytes were used to study the effect of melatonin in response to LPS. Indicators of myocardial and mitochondria injury including mitochondrial membrane potential, mitochondrial permeability transition pore, calcium loading, ROS, and ATP detection were assessed. In addition cell viability and apoptosis as well as autophagy-associated proteins were evaluated. Melatonin was able to protect heart function from LPS, which weakened in the UCP2-knockout mice. Consistently, genipin, a pharmacologic inhibitor of UCP2, augmented LPS-induced damage of AC16 cells. In contrast, melatonin upregulated UCP2 expression and protected the cells from the changes in morphology, mitochondrial membrane potential loss, mitochondrial Ca
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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.