ArticleBMC cardiovascular disorders2023
Protective effects of melatonin on myocardial microvascular endothelial cell injury under hypertensive state by regulating Mst1.
Article in BMC cardiovascular disorders, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Melatonin ameliorates inflammation and improves outcomes of ischemia/reperfusion injury in patients undergoing coronary artery bypass grafting surgery: a randomized placebo-controlled study.Apoptosis : an international journal on programmed cell death · 2025Trial
- MST1 modulates inflammatory responses by targeting the NF-κB/NLRP3 pathway in LPS-induced acute lung injury.Histochemistry and cell biology · 2025Article
- Vascular Pathogenesis in Acute and Long COVID: Current Insights and Therapeutic Outlook.Seminars in thrombosis and hemostasis · 2025Review
- Programmed cell death and melatonin: A comprehensive review.Functional & integrative genomics · 2024Review
- Harmful Free Radicals in Aging: A Narrative Review of Their Detrimental Effects on Health.Indian journal of clinical biochemistry : IJCB · 2024Review
- New Perspectives on the Role and Therapeutic Potential of Melatonin in Cardiovascular Diseases.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2024Review
- Natural compounds targeting mitochondrial dysfunction: emerging therapeutics for target organ damage in hypertension.Frontiers in pharmacology · 2023Review
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study explored the protective effects of melatonin on the hypertensive model in myocardial microvascular endothelial cells.
methodsMouse myocardial microvascular endothelial cells were intervened with angiotensin II to establish hypertensive cell model and divided into control, hypertension (HP), hypertension + adenovirus negative control (HP + Ad-NC), hypertension + adenovirus carrying Mst1 (HP + Ad-Mst1), hypertension + melatonin (HP + MT), hypertension + adenovirus negative control + melatonin (HP + Ad-NC + MT), and hypertension + adenovirus carrying Mst1 + melatonin (HP + Ad-Mst1 + MT) groups. Autophagosomes were observed by transmission electron microscope. Mitochondrial membrane potential was detected by JC-1 staining. Apoptosis was detected by flow cytometry. Oxidative stress markers of MDA, SOD and GSH-PX were measured. The expression of LC3 and p62 was detected by immunofluorescence. Expression levels of Mst1, p-Mst1, Beclin1, LC3, and P62 were detected with Western blot.
resultsCompared with the control group, the autophagosomes in HP, HP + Ad-Mst1, and HP + Ad-NC groups were significantly reduced. Compared with HP group, the autophagosomes in HP + Ad-Mst1 group were significantly reduced. The apoptosis of HP + MT group was significantly lower than HP group. Compared with HP + Ad-Mst1 group, the apoptosis of HP + Ad-Mst1 + MT group was significantly reduced. The ratio of JC-1 monomer in HP + MT group was significantly lower than HP group. Compared with HP + Ad-Mst1 group, the mitochondrial membrane potential of HP + Ad-Mst1 + MT group was also significantly reduced. MDA content in HP + MT group was significantly reduced, but SOD and GSH-PX activities were significantly increased. Compared with HP + Ad-Mst1 group, MDA content in HP + Ad-Mst1 + MT group was significantly reduced, whereas SOD and GSH-PX activities were increased significantly. Mst1 and p-Mst1 proteins in HP + MT group were significantly reduced. Compared with HP + Ad-Mst1 group, Mst1 and p-Mst1 in HP + Ad-Mst1 + MT group were reduced. P62 level was significantly decreased, while Beclin1 and LC3II levels were significantly increased. P62 in HP + MT group was significantly reduced, while Beclin1 and LC3II were significantly increased. Compared with HP + Ad-Mst1 group, P62 in HP + Ad-Mst1 + MT group was significantly reduced, but Beclin1 and LC3II were significantly increased.
conclusionMelatonin may inhibit apoptosis, increase mitochondrial membrane potential, and increase autophagy of myocardial microvascular endothelial cells under hypertensive state via inhibiting Mst1 expression, thereby exerting myocardial protective effect.
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