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Article ; Online: Obesity in Hypertension: The Role of the Expanding Waistline Over the Years and Insights Into the Future.

Jia, Guanghong / Sowers, James R / Whaley-Connell, Adam T

Hypertension (Dallas, Tex. : 1979)

2023 Volume 81, Issue 4, Page(s) 687–690

MeSH term(s)	Humans ; Obesity/complications ; Obesity/epidemiology ; Hypertension/epidemiology ; Hypertension/etiology
Language	English
Publishing date	2023-11-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	423736-5
ISSN	1524-4563 ; 0194-911X ; 0362-4323
ISSN (online)	1524-4563
ISSN	0194-911X ; 0362-4323
DOI	10.1161/HYPERTENSIONAHA.123.21719
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Article ; Online: Diabetic Vasculopathy: Molecular Mechanisms and Clinical Insights.

Jia, George / Bai, Hetty / Mather, Bethany / Hill, Michael A / Jia, Guanghong / Sowers, James R

International journal of molecular sciences

2024 Volume 25, Issue 2

Abstract: Clinical and basic studies have documented that both hyperglycemia and insulin-resistance/hyperinsulinemia not only constitute metabolic disorders contributing to cardiometabolic syndrome, but also predispose to diabetic vasculopathy, which refers to ... ...

Abstract	Clinical and basic studies have documented that both hyperglycemia and insulin-resistance/hyperinsulinemia not only constitute metabolic disorders contributing to cardiometabolic syndrome, but also predispose to diabetic vasculopathy, which refers to diabetes-mellitus-induced microvascular and macrovascular complications, including retinopathy, neuropathy, atherosclerosis, coronary artery disease, hypertension, and peripheral artery disease. The underlying molecular and cellular mechanisms include inappropriate activation of the renin angiotensin-aldosterone system, mitochondrial dysfunction, excessive oxidative stress, inflammation, dyslipidemia, and thrombosis. These abnormalities collectively promote metabolic disorders and further promote diabetic vasculopathy. Recent evidence has revealed that endothelial progenitor cell dysfunction, gut dysbiosis, and the abnormal release of extracellular vesicles and their carried microRNAs also contribute to the development and progression of diabetic vasculopathy. Therefore, clinical control and treatment of diabetes mellitus, as well as the development of novel therapeutic strategies are crucial in preventing cardiometabolic syndrome and related diabetic vasculopathy. The present review focuses on the relationship between insulin resistance and diabetes mellitus in diabetic vasculopathy and related cardiovascular disease, highlighting epidemiology and clinical characteristics, pathophysiology, and molecular mechanisms, as well as management strategies.
MeSH term(s)	Humans ; Diabetic Angiopathies ; Metabolic Syndrome ; Peripheral Vascular Diseases ; Insulin Resistance ; Atherosclerosis ; Diabetes Mellitus
Language	English
Publishing date	2024-01-09
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25020804
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Article ; Online: Vascular endothelial mineralocorticoid receptors and epithelial sodium channels in metabolic syndrome and related cardiovascular disease.

Jia, Guanghong / Hill, Michael A / Sowers, James R

Journal of molecular endocrinology

2023 Volume 71, Issue 3

Abstract: Metabolic syndrome is a group of risk factors that increase the risk of developing metabolic and cardiovascular disease (CVD) and include obesity, dyslipidemia, insulin resistance, atherosclerosis, hypertension, coronary artery disease, and heart failure. ...

Abstract	Metabolic syndrome is a group of risk factors that increase the risk of developing metabolic and cardiovascular disease (CVD) and include obesity, dyslipidemia, insulin resistance, atherosclerosis, hypertension, coronary artery disease, and heart failure. Recent research indicates that excessive production of aldosterone and associated activation of mineralocorticoid receptors (MR) impair insulin metabolic signaling, promote insulin resistance, and increase the risk of developing metabolic syndrome and CVD. Moreover, activation of specific epithelial sodium channels (ENaC) in endothelial cells (EnNaC), which are downstream targets of endothelial-specific MR (ECMR) signaling, are also believed to play a crucial role in the development of metabolic syndrome and CVD. These adverse effects of ECMR/EnNaC activation are mediated by increased oxidative stress, inflammation, and lipid metabolic disorders. It is worth noting that ECMR/EnNaC activation and the pathophysiology underlying metabolic syndrome and CVD appears to exhibit sexual dimorphism. Targeting ECMR/EnNaC signaling may have a beneficial effect in preventing insulin resistance, diabetes, metabolic syndrome, and related CVD. This review aims to examine our current understanding of the relationship between MR activation and increased metabolic syndrome and CVD, with particular emphasis placed on the role for endothelial-specific ECMR/EnNaC signaling in these pathological processes.
MeSH term(s)	Humans ; Metabolic Syndrome ; Cardiovascular Diseases/etiology ; Receptors, Mineralocorticoid ; Insulin Resistance ; Epithelial Sodium Channels ; Endothelial Cells
Chemical Substances	Receptors, Mineralocorticoid ; Epithelial Sodium Channels
Language	English
Publishing date	2023-09-13
Publishing country	England
Document type	Review ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	645012-x
ISSN	1479-6813 ; 0952-5041
ISSN (online)	1479-6813
ISSN	0952-5041
DOI	10.1530/JME-23-0066
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Article ; Online: Tuning Bienenstock-Cooper-Munro learning rules in a two-terminal memristor for neuromorphic computing.

Li, Zeyang / Liu, Peilin / Yang, Guanghong / Jia, Caihong / Zhang, Weifeng

Physical chemistry chemical physics : PCCP

2023 Volume 25, Issue 23, Page(s) 15920–15928

Abstract: In memristors, the implementation of the Bienenstock-Cooper-Munro (BCM) learning rule plays a significant role in the modulation balance of artificial synapses and the reduction of energy consumption owing to their sliding frequency threshold. At present, ...

Abstract	In memristors, the implementation of the Bienenstock-Cooper-Munro (BCM) learning rule plays a significant role in the modulation balance of artificial synapses and the reduction of energy consumption owing to their sliding frequency threshold. At present, the BCM learning rule is mostly achieved by adjusting gating voltage or channel current in field effect transistors. However, owing to the lack of the tunable degrees of freedom, the progress of two-terminal memristors is limited to simulating the BCM learning rule. In this study, by adjusting the series resistance, three types of BCM-like learning rules are found in a two-terminal BaTiO
Language	English
Publishing date	2023-06-15
Publishing country	England
Document type	Journal Article
ZDB-ID	1476244-4
ISSN	1463-9084 ; 1463-9076
ISSN (online)	1463-9084
ISSN	1463-9076
DOI	10.1039/d3cp01134h
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Article ; Online: Hypertension in Diabetes: An Update of Basic Mechanisms and Clinical Disease.

Jia, Guanghong / Sowers, James R

Hypertension (Dallas, Tex. : 1979)

2021 Volume 78, Issue 5, Page(s) 1197–1205

Abstract: Epidemiological studies have documented that insulin resistance and diabetes not only constitute metabolic abnormalities but also predispose to hypertension, vascular stiffness, and associated cardiovascular disease. Meanwhile, excessive arterial ... ...

Abstract	Epidemiological studies have documented that insulin resistance and diabetes not only constitute metabolic abnormalities but also predispose to hypertension, vascular stiffness, and associated cardiovascular disease. Meanwhile, excessive arterial stiffness and impaired vasorelaxation, in turn, contribute to worsening insulin resistance and the development of diabetes. Molecular mechanisms promoting hypertension in diabetes include inappropriate activation of the renin-angiotensin-aldosterone system and sympathetic nervous system, mitochondria dysfunction, excessive oxidative stress, and systemic inflammation. This review highlights recent studies which have uncovered new underlying mechanisms for the increased propensity for the development of hypertension in association with diabetes. These include enhanced activation of epithelial sodium channels, alterations in extracellular vesicles and their microRNAs, abnormal gut microbiota, and increased renal sodium-glucose cotransporter activity, which collectively predispose to hypertension in association with diabetes. This review also covers socioeconomic factors and currently recommended blood pressure targets and related treatment strategies in diabetic patients with hypertension.
MeSH term(s)	Blood Pressure/physiology ; Cardiovascular Diseases/physiopathology ; Diabetes Mellitus, Type 1/complications ; Diabetes Mellitus, Type 1/physiopathology ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/physiopathology ; Humans ; Hypertension/complications ; Hypertension/physiopathology ; Hypertension/therapy ; Insulin Resistance/physiology ; Life Style ; Risk Factors ; Sodium-Glucose Transporter 2 Inhibitors/therapeutic use
Chemical Substances	Sodium-Glucose Transporter 2 Inhibitors
Language	English
Publishing date	2021-10-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	423736-5
ISSN	1524-4563 ; 0194-911X ; 0362-4323
ISSN (online)	1524-4563
ISSN	0194-911X ; 0362-4323
DOI	10.1161/HYPERTENSIONAHA.121.17981
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Zs.A 1488: Show issues

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Article ; Online: Endothelial cell serum and glucocorticoid regulated kinase 1 (SGK1) mediates vascular stiffening.

Zhang, Liping / Sun, Zhe / Yang, Yan / Mack, Austin / Rodgers, Mackenna / Aroor, Annayya / Jia, Guanghong / Sowers, James R / Hill, Michael A

Metabolism: clinical and experimental

2024 Volume 154, Page(s) 155831

Abstract: Background: Excessive dietary salt intake increases vascular stiffness in humans, especially in salt-sensitive populations. While we recently suggested that the endothelial sodium channel (EnNaC) contributes to salt-sensitivity related endothelial cell ( ...

Abstract	Background: Excessive dietary salt intake increases vascular stiffness in humans, especially in salt-sensitive populations. While we recently suggested that the endothelial sodium channel (EnNaC) contributes to salt-sensitivity related endothelial cell (EC) and arterial stiffening, mechanistic understanding remains incomplete. This study therefore aimed to explore the role of EC-serum and glucocorticoid regulated kinase 1 (SGK1), as a reported regulator of sodium channels, in EC and arterial stiffening. Methods and results: A mouse model of salt sensitivity-associated vascular stiffening was produced by subcutaneous implantation of slow-release deoxycorticosterone acetate (DOCA) pellets, with salt (1 % NaCl, 0.2 % KCl) administered via drinking water. Preliminary data showed that global SGK1 deletion caused significantly decreased blood pressure (BP), EnNaC activity and aortic endothelium stiffness as compared to control mice following DOCA-salt treatment. To probe EC signaling pathways, selective deletion of EC-SGK1 was performed by cross-breeding cadherin 5-Cre mice with sgk1 Conclusion: EC-SGK1 contributes to salt-sensitivity related EC and aortic stiffening by mechanisms appearing to involve regulation of actin polymerization.
MeSH term(s)	Animals ; Humans ; Mice ; Actins/metabolism ; Aldosterone/metabolism ; Aldosterone/pharmacology ; Blood Pressure/physiology ; Desoxycorticosterone Acetate ; Endothelial Cells/metabolism ; Glucocorticoids/metabolism ; Vascular Stiffness ; Protein Serine-Threonine Kinases/metabolism ; Immediate-Early Proteins/metabolism
Chemical Substances	Actins ; Aldosterone (4964P6T9RB) ; Desoxycorticosterone Acetate (6E0A168OB8) ; Glucocorticoids ; serum-glucocorticoid regulated kinase (EC 2.7.11.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Immediate-Early Proteins
Language	English
Publishing date	2024-02-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	80230-x
ISSN	1532-8600 ; 0026-0495
ISSN (online)	1532-8600
ISSN	0026-0495
DOI	10.1016/j.metabol.2024.155831
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Article ; Online: Cell-Specific Targeting of the Endothelium in the Cardiorenal Syndrome.

Laham-Karam, Nihay / Laakkonen, Johanna P / Ylä-Herttuala, Seppo / Aroor, Annayya / Jia, Guanghong / Whaley-Connell, Adam

Cardiorenal medicine

2024 Volume 14, Issue 1, Page(s) 129–135

Abstract: Background: The vascular endothelium serves as a semi-selective permeable barrier as a conduit for transport of fluid, solutes, and various cell populations between the vessel lumen and tissues. The endothelium thus has a dynamic role in the regulation ... ...

Abstract	Background: The vascular endothelium serves as a semi-selective permeable barrier as a conduit for transport of fluid, solutes, and various cell populations between the vessel lumen and tissues. The endothelium thus has a dynamic role in the regulation of coagulation, immune system, lipid and electrolyte transport, as well as neurohumoral influences on vascular tone and end-organ injury to tissues such as the heart and kidney. Summary: Within this framework, pharmacologic strategies for heart and kidney diseases including blood pressure, glycemic control, and lipid reduction provide significant risk reduction, yet certain populations are at risk for substantial residual risk for disease progression and treatment resistance and often have unwanted off-target effects leaving the need for adjunct, alternative targeted therapies. Recent advances in techniques in sequencing and spatial transcriptomics have paved the way for the development of new therapies for targeting heart and kidney disease that include various gene, cell, and nano-based therapies. Cell-specific endothelium-specific targeting of viral vectors will enable their use for the treatment of heart and kidney diseases with gene therapy that can avoid unwanted off-target effects, improve treatment resistance, and reduce residual risk for disease progression. Key messages: The vascular endothelium is an important therapeutic target for chronic kidney and cardiovascular diseases. Developing endothelial-specific gene therapies can benefit patients who develop resistance to current treatments.
MeSH term(s)	Humans ; Cardio-Renal Syndrome/physiopathology ; Cardio-Renal Syndrome/metabolism ; Endothelium, Vascular/physiopathology ; Endothelium, Vascular/metabolism ; Genetic Therapy/methods ; Animals
Language	English
Publishing date	2024-02-09
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2595659-0
ISSN	1664-5502 ; 1664-3828
ISSN (online)	1664-5502
ISSN	1664-3828
DOI	10.1159/000537764
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Article ; Online: Targeting endothelial exosomes for the prevention of cardiovascular disease.

Jia, Guanghong / Sowers, James R

Biochimica et biophysica acta. Molecular basis of disease

2020 Volume 1866, Issue 8, Page(s) 165833

Abstract: Exosomes are small lipid bilayer-enclosed 30-140 nm diameter vesicles formed from endosomes. Exosomes are secreted by various cell types including endothelial cells, immune cells and other cardiovascular tissues, and they can be detected in plasma, urine, ...

Abstract	Exosomes are small lipid bilayer-enclosed 30-140 nm diameter vesicles formed from endosomes. Exosomes are secreted by various cell types including endothelial cells, immune cells and other cardiovascular tissues, and they can be detected in plasma, urine, cerebrospinal fluid, as well as tissues. Exosomes were initially regarded as a disposal mechanism to discard unwanted materials from cells. Recent studies suggest that exosomes play an important role in mediating of intercellular communication through the delivery and transport of cellular components such as nucleic acids, lipids, and proteins and thus regulate cardiovascular disease. Further, the underlying mechanisms by which abnormally released exosomes promote cardiovascular disease are not well understood. This review highlights recent studies involving endothelial exosomes, gives a brief overview of exosome biogenesis and release, isolation and identification of exosomes, and provides a contemporary understanding of the endothelial exosome pathophysiology and potential therapeutic strategies.
MeSH term(s)	Antigens, CD/genetics ; Antigens, CD/metabolism ; Biological Transport ; Biomarkers/metabolism ; Calcium-Binding Proteins/genetics ; Calcium-Binding Proteins/metabolism ; Cardiovascular Diseases/genetics ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/pathology ; Cardiovascular Diseases/prevention & control ; Cell Communication ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Cell- and Tissue-Based Therapy/methods ; Drug Carriers/therapeutic use ; Endosomal Sorting Complexes Required for Transport/genetics ; Endosomal Sorting Complexes Required for Transport/metabolism ; Endothelial Cells/chemistry ; Endothelial Cells/metabolism ; Exosomes/genetics ; Exosomes/metabolism ; Exosomes/transplantation ; Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Molecular Targeted Therapy/methods ; Organelle Biogenesis ; RNA, Small Interfering/therapeutic use
Chemical Substances	Antigens, CD ; Biomarkers ; Calcium-Binding Proteins ; Cell Cycle Proteins ; Drug Carriers ; Endosomal Sorting Complexes Required for Transport ; MicroRNAs ; PDCD6IP protein, human ; RNA, Small Interfering
Language	English
Publishing date	2020-05-04
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	60-7
ISSN	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2020.165833
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Article ; Online: An efficient privacy-preserving blockchain storage method for internet of things environment.

Jia, Dayu / Yang, Guanghong / Huang, Min / Xin, Junchang / Wang, Guoren / Yuan, George Y

World wide web

2023 , Page(s) 1–18

Abstract: Blockchain is a key technology to realize decentralized trust management. In recent studies, sharding-based blockchain models are proposed and applied to the resource-constrained Internet of Things (IoT) scenario, and machine learning-based models are ... ...

Abstract	Blockchain is a key technology to realize decentralized trust management. In recent studies, sharding-based blockchain models are proposed and applied to the resource-constrained Internet of Things (IoT) scenario, and machine learning-based models are presented to improve the query efficiency of the sharding-based blockchains by classifying hot data and storing them locally. However, in some scenarios, these presented blockchain models cannot be deployed because the block features used as input in the learning method are privacy. In this paper, we propose an efficient privacy-preserving blockchain storage method for the IoT environment. The new method classifies hot blocks based on the federated extreme learning machine method and saves the hot blocks through one of the sharded blockchain models called ElasticChain. The features of hot blocks will not be read by other nodes in this method, and user privacy is effectively protected. Meanwhile, hot blocks are saved locally, and data query speed is improved. Furthermore, in order to comprehensively evaluate a hot block, five features of hot blocks are defined, including objective feature, historical popularity, potential popularity, storage requirements and training value. Finally, the experimental results on synthetic data demonstrate the accuracy and efficiency of the proposed blockchain storage model.
Language	English
Publishing date	2023-05-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	2025142-7
ISSN	1573-1413 ; 1386-145X
ISSN (online)	1573-1413
ISSN	1386-145X
DOI	10.1007/s11280-023-01172-0
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Article ; Online: Increased Fibro-Adipogenic Progenitors and Intramyocellular Lipid Accumulation in Obesity-Related Skeletal Muscle Dysfunction.

Jia, Guanghong / Sowers, James R

Diabetes

2018 Volume 68, Issue 1, Page(s) 18–20

MeSH term(s)	Adipogenesis ; Diaphragm ; Humans ; Lipids ; Muscle, Skeletal ; Obesity
Chemical Substances	Lipids
Language	English
Publishing date	2018-12-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/dbi18-0047
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