Cited by 550Diabetes Treatment and ManagementCardiovascular Function and Risk FactorsMitochondrial Function and Pathology

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Empagliflozin rescues diabetic myocardial microvascular injury via AMPK-mediated inhibition of mitochondrial fission

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Zhou, Hao, Wang, Shuyi, Zhu, Pingjun, Hu, Shunying, Chen, Yundai, Ren, Jun·2018·Redox Biology

DOI 10.1016/j.redox.2017.12.019PMC PMC5756062

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Abstract

Impaired cardiac microvascular function contributes to diabetic cardiovascular complications although effective therapy remains elusive. Empagliflozin, a sodium-glucose cotransporter 2 (SGLT2) inhibitor recently approved for treatment of type 2 diabetes, promotes glycosuria excretion and offers cardioprotective actions beyond its glucose-lowering effects. This study was designed to evaluate the effect of empagliflozin on cardiac microvascular injury in diabetes and the underlying mechanism involved with a focus on mitochondria. Our data revealed that empagliflozin improved diabetic myocardial structure and function, preserved cardiac microvascular barrier function and integrity, sustained eNOS phosphorylation and endothelium-dependent relaxation, as well as improved microvessel density and perfusion. Further study suggested that empagliflozin exerted its effects through inhibition of mitochondrial fission in an adenosine monophosphate (AMP)-activated protein kinase (AMPK)-dependent manner. Empagliflozin restored AMP-to-ATP ratio to trigger AMPK activation, suppressed Drp1 S616 phosphorylation, and increased Drp1 S637 phosphorylation, ultimately leading to inhibition of mitochondrial fission. The empagliflozin-induced inhibition of mitochondrial fission preserved cardiac microvascular endothelial cell (CMEC) barrier function through suppressed mitochondrial reactive oxygen species (mtROS) production and subsequently oxidative stress to impede CMEC senescence. Empagliflozin-induced fission loss also favored angiogenesis by promoting CMEC migration through amelioration of F-actin depolymerization. Taken together, these results indicated the therapeutic promises of empagliflozin in the treatment of pathological microvascular changes in diabetes.

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RETRACTED: Effects of melatonin on fatty liver disease: The role of NR 4A1/ DNA ‐ PK cs/p53 pathway, mitochondrial fission, and mitophagy
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Empagliflozin, Cardiovascular Outcomes, and Mortality in Type 2 Diabetes
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AMP-activated protein kinase mediates mitochondrial fission in response to energy stress
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Background
The Interplay between MiR-134/BDNF and LKB1/AMPK/SIRT1 Accentuates the Antidepressant Efficacy of Empagliflozin in Ovariectomized Rats
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Recombinant Human Growth Hormone Inhibits Lipotoxicity, Oxidative Stress, and Apoptosis in a Mouse Model of Diabetic Cardiomyopathy
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Empagliflozin, a sodium‐glucose cotransporter inhibitor enhancing mitochondrial action and cardioprotection in metabolic syndrome
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“In fact, the role of EMPA in promoting mitophagy is mainly through AMPK, FUNDC1, NIX/BNIP3L, Drp1, mTOR, Beclin ‐ 1 and other signaling pathways or molecules (Cai, Guo, et al., 2022; Cai, Wu, et al., 2022; Korbut et al., 2020; Sun et al., 2020; Wang et al., 2020; Zhou et al., 2018).”
Background
EMP1 knockdown mitigated high glucose‐induced pyroptosis and oxidative stress in rat H9c2 cardiomyocytes by inhibiting the RAS/RAF/MAPK signaling pathway
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Total Glucosides of Peony Protect Cardiomyocytes against Oxidative Stress and Inflammation by Reversing Mitochondrial Dynamics and Bioenergetics
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Background
Retracted
RETRACTED: Matrine Protects Cardiomyocytes Against Hyperglycemic Stress by Promoting Mitofusin 2-Induced Mitochondrial Fusion
Xiao, T., Huang, J., Liu, Y., Zhao, Y., & Wei, M. (2021) · Frontiers in Physiology · doi:10.3389/fphys.2020.597429 · Cited by 3
Retracted
Protective or Inhibitory Effect of Pharmacological Therapy on Cardiac Ischemic Preconditioning: A Literature Review
de Paula, L. J. C., Uchida, A. H., Rezende, P. C., Soares, P. R., & Scudeler, T. L. (2022) · Current Vascular Pharmacology · doi:10.2174/1570161120666220819163025 · Cited by 3
Retraction Note to: Excessive mitochondrial fragmentation triggered by erlotinib promotes pancreatic cancer PANC‑1 cell apoptosis via activating the mROS‑HtrA2/Omi pathways
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The mitochondrial protective mechanisms mediated by SGLT2i: from molecular basis to clinical implications
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Neuroprotective Potential of SGLT2 Inhibitors in Animal Models of Alzheimer’s Disease and Type 2 Diabetes Mellitus: A Systematic Review
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“Additionally, empagliflozin [55] and dapagliflozin [31] promote mitochondrial fusion by increasing the expression of mitofusin-1 (MFN1) and mitofusin-2 (MFN2) proteins in T2DM animal models; these processes are crucial for maintaining mitochondrial integrity and function [56].”
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Molecular Mechanisms and Clinical Evidence Supporting the Four Pillars of Therapy in Diabetic Kidney Disease: Emerging Therapeutic Perspectives
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Empagliflozin mitigated cisplatin induced renal endothelial dysfunction in rats via repressing oxidative, inflammatory, apoptotic and fibrotic signals
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Cardiac-derived CTRP9 mediates the protection of empagliflozin against diabetes-induced male subfertility in mice
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Advances in Cardiovascular Pharmacotherapy. IV. Sodium-Glucose Cotransporter Type 2 Inhibitors, Part 2: Mechanisms for Myocardial Protection, Adverse Effects, and Perioperative Implications
Pagel, P. S., Hang, D., Freed, J. K., & Crystal, G. J. (2025) · Journal of Cardiothoracic and Vascular Anesthesia · doi:10.1053/j.jvca.2025.06.015 · Cited by 2
Metabolic Regulation of Mitochondrial Dynamics and Cardiac Function
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Mitofusin-2 gene polymorphisms and metabolic dysfunction associated fatty liver disease: a case-control study in a Chinese population
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Potential Role of SGLT2 Inhibitors in the Treatment and Prevention of Diabetic Cardiomyopathy
Nandave, M. (2024) · Springer eBooks · doi:10.1007/978-981-97-7568-2_5 · Cited by 2
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Dapagliflozin Restores Diabetes-Associated Decline in Vasculogenic Capacity of Endothelial Progenitor Cells via Activating AMPK-Mediated Inhibition of Inflammation and Oxidative StressPreprint
Luo, L., Dong, B., Zhang, J., Qiu, Y., Liu, X., Zhou, Z. C., He, J., Zhang, X., Chen, L., & Xia, W. (2021) · Research Square · doi:10.21203/rs.3.rs-694662/v1 · Cited by 2
Mechanisms of SGLT2 Inhibitors in the Treatment of Myocardial Ischemia-Reperfusion Injury in Animal Models
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Exploring the Evolving Role of SGLT-2 Inhibitors and GLP-1 Receptor Agonists in Managing Cardiovascular Injury Induced by Obesity: Spotlight on ROS as a Key Mediator
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Roles of Empagliflozin in Diabetic Cardiomyopathy: A Review
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Sirt1/Drp1 Pathway Reduces Microvascular Endothelial Cell Injury in Diabetic Pateints’ Hearts by Inhibiting Excessive Mitochondrial Division
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“…tubuloglomerular feedback, which reduces glomerular hyperfiltration and intraglomerular pressure, particularly in patients with diabetes or CKD. [10,16] Finally, by increasing ketone body availability, SGLT2 inhibitors enhance myocardial energy efficiency, providing a more oxygen-sparing…”
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Dapagliflozin attenuates hypothyroidism induced liver and lung dysfunction via regulation of mitophagy and apoptosis
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Targeted metabolomics to assess positive effects of empagliflozin in a Parkinson’s disease model: focused on the kynurenine pathway and oxidative stress
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Human iPSC-derived engineered heart tissue model of diastolic dysfunction in heart failure with preserved ejection fraction
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D-beta-hydroxybutyrate reduced the enhanced cardiac microvascular endothelial FoxO1 to play protective roles in diabetic rats and high glucose-stimulated human cardiac microvascular endothelial cells
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[Empagliflozin alleviates cardiac microvascular ischemia/reperfusion injury by maintaining myocardial mitochondrial homeostasis].
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Retraction Note to: IL‑2 augments the sorafenib‑induced apoptosis in liver cancer by promoting mitochondrial fission and activating the JNK/TAZ pathway
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Retracted
Dapagliflozin restores diabetes-associated decline in vasculogenic capacity of endothelial progenitor cells via activating AMPK-mediated inhibition of inflammation and oxidative stressPreprint
Luo, L., Dong, B., Zhang, J., Qiu, Y., Liu, X., Zhou, Z. C., He, J., Zhang, X., Chen, L., & Xia, W. (2022) · Research Square · doi:10.21203/rs.3.rs-694662/v2 · Cited by 1
Direct cardial effects and mechanisms of cardiovascular action of gliflosins
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Authors: Zhou, H., Wang, S., Zhu, P., Hu, S., Chen, Y., & Ren, J.
Affiliations: Chinese PLA General Hospital (CN)
University of Wyoming (US)
Corresponding author: Zhou, Hao
Chen, Yundai
Ren, Jun
ORCID: Zhou, Hao
Wang, Shuyi
Zhu, Pingjun
Hu, Shunying
Chen, Yundai
Ren, Jun
Venue: Redox Biology
Publisher: Elsevier BV
Published: 2018-05
Volume: 15
Pages: 335-346
ISSN: 2213-2317 (ISSN-L)
DOI: 10.1016/j.redox.2017.12.019
PMC: PMC5756062
OpenAlex: W2777514005
Cited by: 550
References: 63
Citations by year: 2026: 34 · 2025: 53 · 2024: 87 · 2023: 71 · 2022: 71 · 2021: 65 · 2020: 63 · 2019: 53 · 2018: 50
FWCI: 35.91
Type: journal article
Language: en
Update notices: erratum (2024-05-01)
Open access: gold
doi.org
Licence: cc-by-nc-nd
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
creativecommons.org/licenses/by-nc-nd/4.0/ (vor)
Locations: Redox Biology (publishedVersion, cc-by-nc-nd)
PubMed Central (publishedVersion, cc-by-nc-nd)
PubMed (publishedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders: National Natural Science Foundation of China (81441008, 81030002, 81102079, 81270186)
Topics: Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords: empagliflozin, SGLT2 inhibitors, diabetic cardiomyopathy, mitochondrial fission, AMPK, Drp1 phosphorylation, endothelial barrier function, endothelial cell senescence, mitochondrial reactive oxygen species, oxidative stress, angiogenesis, endothelial cell migration, F-actin depolymerization, eNOS phosphorylation, type 2 diabetes
MeSH terms: AMP-Activated Protein Kinase Kinases, Animals, Benzhydryl Compounds, Diabetes Mellitus, Type 2, Glucosides, Heart Injuries, Humans, Mitochondria, Protein Kinases, Endothelial Cells, Mice, Mitochondrial Dynamics

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Empagliflozin rescues diabetic myocardial microvascular injury via AMPK-mediated inhibition of mitochondrial fission

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