Hypoglycemia Induces Diabetic Macrovascular Endothelial Dysfunction via Endothelial Cell PANoptosis, Macrophage Polarization, and VSMC Fibrosis

Hypoglycemia is a commonly neglected complication in elderly diabetic patients, which can lead to cardiovascular events. Endothelial cell dysfunction is the primary inducer of cardiovascular events, and it is associated with hypoglycemia‐triggered cytokine release and inflammatory programmed cell de...

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Vydané v:Advanced science Ročník 12; číslo 37; s. e14530 - n/a
Hlavní autori: Zuo, Deyu, Peng, Yuce, Zhao, Guozhi, Cheng, Zhesheng, Luo, Minghao, Lv, Dingyi, Chang, Shuting, Li, Na, Huang, Yanyao, Li, Xunjia, He, An
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: Germany John Wiley & Sons, Inc 01.10.2025
Wiley
Predmet:
ANGPTL4
Animals
Atherosclerosis
Cardiovascular disease
Cell death
Coronary vessels
Diabetes
Diabetes Mellitus, Experimental - metabolism
Diabetic Angiopathies - metabolism
Endothelial Cells - metabolism
Endothelial Cells - pathology
Endothelium
Endothelium, Vascular - metabolism
Endothelium, Vascular - pathology
Fibrosis
Gene expression
Humans
Hypoglycemia
Hypoglycemia - complications
Hypoglycemia - metabolism
Inflammation
Macrophages - metabolism
Macrophages - pathology
Male
Mice
Mice, Inbred C57BL
Molecular biology
Mortality
Muscle, Smooth, Vascular - metabolism
Muscle, Smooth, Vascular - pathology
PANoptosis
proinflammatory polarization
Proteins
proinflammatory polarization
fibrosis
ANGPTL4
PANoptosis
hypoglycemia
ISSN:2198-3844, 2198-3844
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Abstract Hypoglycemia is a commonly neglected complication in elderly diabetic patients, which can lead to cardiovascular events. Endothelial cell dysfunction is the primary inducer of cardiovascular events, and it is associated with hypoglycemia‐triggered cytokine release and inflammatory programmed cell death. A comprehensive understanding of lineage‐specific variations in pathological vascular changes is essential to mitigate cardiovascular events and ensure therapeutic efficacy. Herein, unbiased clustering analyses and single‐nucleus RNA sequencing are performed on cells of the thoracic aorta in db/db and insulin‐induced hypoglycemic db/db mice. Comparative analyses show changes in lineage‐specific genes, subpopulation composition, intercellular communication, and molecular biology in hypoglycemic diabetic mice. The analyses also revealed the changes of different cells, particularly endothelial cell PANoptosis, macrophage inflammatory polarization, and vascular smooth muscle cell (VSMC) fibrosis. Pseudo‐time sequencing, differential expression, and regulation network analyses revealed the association of potential hub genes Klf2, ETS2, Elavl1, C3, and Nr4a1 with the mentioned pathological processes. It is demonstrated that hypoglycemia induces VSMC fibrosis in vivo, whereas Angptl4 knockdown can attenuate VSMC fibrosis in vitro. These findings demonstrate the hypoglycemic macroangiopathy mechanism and provide important references for future disease intervention and treatment. This study investigates hypoglycemia‐induced diabetic macrovascular endothelial dysfunction. It reveals that hypoglycemia triggers ZBP1‐dependent PANoptosis of endothelial cells, proinflammatory polarization of macrophages, and fibrosis of vascular smooth muscle cells (VSMCs) in diabetic mice. Key regulators are identified, with ANGPTL4 validated as a pro‐fibrotic activator. The findings elucidate cellular mechanisms and offer therapeutic insights for hypoglycemia‐related cardiovascular events.
AbstractList Hypoglycemia is a commonly neglected complication in elderly diabetic patients, which can lead to cardiovascular events. Endothelial cell dysfunction is the primary inducer of cardiovascular events, and it is associated with hypoglycemia‐triggered cytokine release and inflammatory programmed cell death. A comprehensive understanding of lineage‐specific variations in pathological vascular changes is essential to mitigate cardiovascular events and ensure therapeutic efficacy. Herein, unbiased clustering analyses and single‐nucleus RNA sequencing are performed on cells of the thoracic aorta in db/db and insulin‐induced hypoglycemic db/db mice. Comparative analyses show changes in lineage‐specific genes, subpopulation composition, intercellular communication, and molecular biology in hypoglycemic diabetic mice. The analyses also revealed the changes of different cells, particularly endothelial cell PANoptosis, macrophage inflammatory polarization, and vascular smooth muscle cell (VSMC) fibrosis. Pseudo‐time sequencing, differential expression, and regulation network analyses revealed the association of potential hub genes Klf2, ETS2, Elavl1, C3, and Nr4a1 with the mentioned pathological processes. It is demonstrated that hypoglycemia induces VSMC fibrosis in vivo, whereas Angptl4 knockdown can attenuate VSMC fibrosis in vitro. These findings demonstrate the hypoglycemic macroangiopathy mechanism and provide important references for future disease intervention and treatment. This study investigates hypoglycemia‐induced diabetic macrovascular endothelial dysfunction. It reveals that hypoglycemia triggers ZBP1‐dependent PANoptosis of endothelial cells, proinflammatory polarization of macrophages, and fibrosis of vascular smooth muscle cells (VSMCs) in diabetic mice. Key regulators are identified, with ANGPTL4 validated as a pro‐fibrotic activator. The findings elucidate cellular mechanisms and offer therapeutic insights for hypoglycemia‐related cardiovascular events.
Hypoglycemia is a commonly neglected complication in elderly diabetic patients, which can lead to cardiovascular events. Endothelial cell dysfunction is the primary inducer of cardiovascular events, and it is associated with hypoglycemia‐triggered cytokine release and inflammatory programmed cell death. A comprehensive understanding of lineage‐specific variations in pathological vascular changes is essential to mitigate cardiovascular events and ensure therapeutic efficacy. Herein, unbiased clustering analyses and single‐nucleus RNA sequencing are performed on cells of the thoracic aorta in db/db and insulin‐induced hypoglycemic db/db mice. Comparative analyses show changes in lineage‐specific genes, subpopulation composition, intercellular communication, and molecular biology in hypoglycemic diabetic mice. The analyses also revealed the changes of different cells, particularly endothelial cell PANoptosis, macrophage inflammatory polarization, and vascular smooth muscle cell (VSMC) fibrosis. Pseudo‐time sequencing, differential expression, and regulation network analyses revealed the association of potential hub genes Klf2 , ETS2 , Elavl1 , C3 , and Nr4a1 with the mentioned pathological processes. It is demonstrated that hypoglycemia induces VSMC fibrosis in vivo, whereas Angptl4 knockdown can attenuate VSMC fibrosis in vitro. These findings demonstrate the hypoglycemic macroangiopathy mechanism and provide important references for future disease intervention and treatment.
Abstract Hypoglycemia is a commonly neglected complication in elderly diabetic patients, which can lead to cardiovascular events. Endothelial cell dysfunction is the primary inducer of cardiovascular events, and it is associated with hypoglycemia‐triggered cytokine release and inflammatory programmed cell death. A comprehensive understanding of lineage‐specific variations in pathological vascular changes is essential to mitigate cardiovascular events and ensure therapeutic efficacy. Herein, unbiased clustering analyses and single‐nucleus RNA sequencing are performed on cells of the thoracic aorta in db/db and insulin‐induced hypoglycemic db/db mice. Comparative analyses show changes in lineage‐specific genes, subpopulation composition, intercellular communication, and molecular biology in hypoglycemic diabetic mice. The analyses also revealed the changes of different cells, particularly endothelial cell PANoptosis, macrophage inflammatory polarization, and vascular smooth muscle cell (VSMC) fibrosis. Pseudo‐time sequencing, differential expression, and regulation network analyses revealed the association of potential hub genes Klf2, ETS2, Elavl1, C3, and Nr4a1 with the mentioned pathological processes. It is demonstrated that hypoglycemia induces VSMC fibrosis in vivo, whereas Angptl4 knockdown can attenuate VSMC fibrosis in vitro. These findings demonstrate the hypoglycemic macroangiopathy mechanism and provide important references for future disease intervention and treatment.
Hypoglycemia is a commonly neglected complication in elderly diabetic patients, which can lead to cardiovascular events. Endothelial cell dysfunction is the primary inducer of cardiovascular events, and it is associated with hypoglycemia-triggered cytokine release and inflammatory programmed cell death. A comprehensive understanding of lineage-specific variations in pathological vascular changes is essential to mitigate cardiovascular events and ensure therapeutic efficacy. Herein, unbiased clustering analyses and single-nucleus RNA sequencing are performed on cells of the thoracic aorta in db/db and insulin-induced hypoglycemic db/db mice. Comparative analyses show changes in lineage-specific genes, subpopulation composition, intercellular communication, and molecular biology in hypoglycemic diabetic mice. The analyses also revealed the changes of different cells, particularly endothelial cell PANoptosis, macrophage inflammatory polarization, and vascular smooth muscle cell (VSMC) fibrosis. Pseudo-time sequencing, differential expression, and regulation network analyses revealed the association of potential hub genes Klf2, ETS2, Elavl1, C3, and Nr4a1 with the mentioned pathological processes. It is demonstrated that hypoglycemia induces VSMC fibrosis in vivo, whereas Angptl4 knockdown can attenuate VSMC fibrosis in vitro. These findings demonstrate the hypoglycemic macroangiopathy mechanism and provide important references for future disease intervention and treatment.Hypoglycemia is a commonly neglected complication in elderly diabetic patients, which can lead to cardiovascular events. Endothelial cell dysfunction is the primary inducer of cardiovascular events, and it is associated with hypoglycemia-triggered cytokine release and inflammatory programmed cell death. A comprehensive understanding of lineage-specific variations in pathological vascular changes is essential to mitigate cardiovascular events and ensure therapeutic efficacy. Herein, unbiased clustering analyses and single-nucleus RNA sequencing are performed on cells of the thoracic aorta in db/db and insulin-induced hypoglycemic db/db mice. Comparative analyses show changes in lineage-specific genes, subpopulation composition, intercellular communication, and molecular biology in hypoglycemic diabetic mice. The analyses also revealed the changes of different cells, particularly endothelial cell PANoptosis, macrophage inflammatory polarization, and vascular smooth muscle cell (VSMC) fibrosis. Pseudo-time sequencing, differential expression, and regulation network analyses revealed the association of potential hub genes Klf2, ETS2, Elavl1, C3, and Nr4a1 with the mentioned pathological processes. It is demonstrated that hypoglycemia induces VSMC fibrosis in vivo, whereas Angptl4 knockdown can attenuate VSMC fibrosis in vitro. These findings demonstrate the hypoglycemic macroangiopathy mechanism and provide important references for future disease intervention and treatment.
Author Cheng, Zhesheng
Zuo, Deyu
Chang, Shuting
Lv, Dingyi
Peng, Yuce
Li, Na
Luo, Minghao
Li, Xunjia
Huang, Yanyao
Zhao, Guozhi
He, An
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  surname: Zuo
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  organization: The First Affiliated Hospital of Chongqing Medical University
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  organization: St. John's University
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  fullname: Luo, Minghao
  organization: Cardiovascular Disease Laboratory of Chongqing Medical University
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  organization: Cardiovascular Disease Laboratory of Chongqing Medical University
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  fullname: Huang, Yanyao
  organization: Cardiovascular Disease Laboratory of Chongqing Medical University
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  surname: Li
  fullname: Li, Xunjia
  email: lixunjia@cqctcm.edu.cn
  organization: Chongqing Precision Medical Industry Technology Research Institute
– sequence: 11
  givenname: An
  surname: He
  fullname: He, An
  email: an.he@hospital.cqmu.edu.cn
  organization: Cardiovascular Disease Laboratory of Chongqing Medical University
BackLink https://www.ncbi.nlm.nih.gov/pubmed/40650639$$D View this record in MEDLINE/PubMed
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Keywords proinflammatory polarization
fibrosis
ANGPTL4
PANoptosis
hypoglycemia
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Snippet Hypoglycemia is a commonly neglected complication in elderly diabetic patients, which can lead to cardiovascular events. Endothelial cell dysfunction is the...
Abstract Hypoglycemia is a commonly neglected complication in elderly diabetic patients, which can lead to cardiovascular events. Endothelial cell dysfunction...
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StartPage e14530
SubjectTerms ANGPTL4
Animals
Atherosclerosis
Cardiovascular disease
Cell death
Coronary vessels
Diabetes
Diabetes Mellitus, Experimental - metabolism
Diabetic Angiopathies - metabolism
Endothelial Cells - metabolism
Endothelial Cells - pathology
Endothelium
Endothelium, Vascular - metabolism
Endothelium, Vascular - pathology
Fibrosis
Gene expression
Humans
Hypoglycemia
Hypoglycemia - complications
Hypoglycemia - metabolism
Inflammation
Macrophages - metabolism
Macrophages - pathology
Male
Mice
Mice, Inbred C57BL
Molecular biology
Mortality
Muscle, Smooth, Vascular - metabolism
Muscle, Smooth, Vascular - pathology
PANoptosis
proinflammatory polarization
Proteins
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Title Hypoglycemia Induces Diabetic Macrovascular Endothelial Dysfunction via Endothelial Cell PANoptosis, Macrophage Polarization, and VSMC Fibrosis
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