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Article: Monocyte and macrophage foam cells in diabetes-accelerated atherosclerosis.

Cervantes, Jocelyn / Kanter, Jenny E

2023 Volume 10, Page(s) 1213177

Abstract: Diabetes results in an increased risk of atherosclerotic cardiovascular disease. This minireview will discuss whether monocyte and macrophage lipid loading contribute to this increased risk, as monocytes and macrophages are critically involved in the ... ...

Abstract	Diabetes results in an increased risk of atherosclerotic cardiovascular disease. This minireview will discuss whether monocyte and macrophage lipid loading contribute to this increased risk, as monocytes and macrophages are critically involved in the progression of atherosclerosis. Both uptake and efflux pathways have been described as being altered by diabetes or conditions associated with diabetes, which may contribute to the increased accumulation of lipids seen in macrophages in diabetes. More recently, monocytes have also been described as lipid-laden in response to elevated lipids, including triglyceride-rich lipoproteins, the class of lipids often elevated in the setting of diabetes.
Language	English
Publishing date	2023-06-12
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2781496-8
ISSN	2297-055X
ISSN	2297-055X
DOI	10.3389/fcvm.2023.1213177
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: FOXP1: A Gatekeeper of Endothelial Cell Inflammation.

Kanter, Jenny E

Circulation research

2019 Volume 125, Issue 6, Page(s) 606–608

MeSH term(s)	Atherosclerosis ; Endothelial Cells ; Forkhead Transcription Factors ; Humans ; Inflammasomes ; Inflammation ; NLR Family, Pyrin Domain-Containing 3 Protein ; Repressor Proteins
Chemical Substances	FOXP1 protein, human ; Forkhead Transcription Factors ; Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; NLRP3 protein, human ; Repressor Proteins
Language	English
Publishing date	2019-08-29
Publishing country	United States
Document type	Editorial ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.119.315687
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Article ; Online: Apolipoprotein C3 and apolipoprotein B colocalize in proximity to macrophages in atherosclerotic lesions in diabetes.

Kanter, Jenny E / Bornfeldt, Karin E

Journal of lipid research

2020 Volume 62, Page(s) 100010

MeSH term(s)	Apolipoprotein C-III
Chemical Substances	Apolipoprotein C-III
Language	English
Publishing date	2020-12-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80154-9
ISSN	1539-7262 ; 0022-2275
ISSN (online)	1539-7262
ISSN	0022-2275
DOI	10.1194/jlr.ILR120001217
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Article ; Online: Monocyte Recruitment Versus Macrophage Proliferation in Atherosclerosis.

Kanter, Jenny E

Circulation research

2017 Volume 121, Issue 10, Page(s) 1109–1110

MeSH term(s)	Apoptosis ; Atherosclerosis ; Cell Proliferation ; Humans ; Lipids ; Macrophages ; Monocytes ; Protein Isoforms
Chemical Substances	Lipids ; Protein Isoforms
Language	English
Publishing date	2017-10-25
Publishing country	United States
Document type	Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.117.311973
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Article ; Online: Quartet of APOCs and the Different Roles They Play in Diabetes.

Hsu, Cheng-Chieh / Kanter, Jenny E / Kothari, Vishal / Bornfeldt, Karin E

Arteriosclerosis, thrombosis, and vascular biology

2023 Volume 43, Issue 7, Page(s) 1124–1133

Abstract: APOA1 and APOB are the structural proteins of high-density lipoprotein and APOB-containing lipoproteins, such as low-density lipoprotein and very low-density lipoprotein, respectively. The 4 smaller APOCs (APOC1, APOC2, APOC3, and APOC4) are exchangeable ...

Abstract	APOA1 and APOB are the structural proteins of high-density lipoprotein and APOB-containing lipoproteins, such as low-density lipoprotein and very low-density lipoprotein, respectively. The 4 smaller APOCs (APOC1, APOC2, APOC3, and APOC4) are exchangeable apolipoproteins; they are readily transferred among high-density lipoproteins and APOB-containing lipoproteins. The APOCs regulate plasma triglyceride and cholesterol levels by modulating substrate availability and activities of enzymes interacting with lipoproteins and by interfering with APOB-containing lipoprotein uptake through hepatic receptors. Of the 4 APOCs, APOC3 has been best studied in relation to diabetes. Elevated serum APOC3 levels predict incident cardiovascular disease and progression of kidney disease in people with type 1 diabetes. Insulin suppresses APOC3 levels, and accordingly, elevated APOC3 levels associate with insulin deficiency and insulin resistance. Mechanistic studies in a mouse model of type 1 diabetes have demonstrated that APOC3 acts in the causal pathway of diabetes-accelerated atherosclerosis. The mechanism is likely due to the ability of APOC3 to slow the clearance of triglyceride-rich lipoproteins and their remnants, thereby causing an increased accumulation of atherogenic lipoprotein remnants in lesions of atherosclerosis. Less is known about the roles of APOC1, APOC2, and APOC4 in diabetes.
MeSH term(s)	Mice ; Animals ; Apolipoprotein C-II ; Diabetes Mellitus, Type 1 ; Lipoproteins ; Triglycerides ; Lipoproteins, HDL/metabolism ; Apolipoprotein C-III ; Lipoproteins, LDL/metabolism ; Atherosclerosis/metabolism ; Apolipoproteins B ; Insulins
Chemical Substances	Apolipoprotein C-II ; Lipoproteins ; Triglycerides ; Lipoproteins, HDL ; Apolipoprotein C-III ; Lipoproteins, LDL ; Apolipoproteins B ; Insulins
Language	English
Publishing date	2023-05-25
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.122.318290
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Article ; Online: Emerging Targets for Cardiovascular Disease Prevention in Diabetes.

Stitziel, Nathan O / Kanter, Jenny E / Bornfeldt, Karin E

Trends in molecular medicine

2020 Volume 26, Issue 8, Page(s) 744–757

Abstract: Type 1 and type 2 diabetes mellitus (T1DM and T2DM) increase the risk of atherosclerotic cardiovascular disease (CVD), resulting in acute cardiovascular events, such as heart attack and stroke. Recent clinical trials point toward new treatment and ... ...

Abstract	Type 1 and type 2 diabetes mellitus (T1DM and T2DM) increase the risk of atherosclerotic cardiovascular disease (CVD), resulting in acute cardiovascular events, such as heart attack and stroke. Recent clinical trials point toward new treatment and prevention strategies for cardiovascular complications of T2DM. New antidiabetic agents show unexpected cardioprotective benefits. Moreover, genetic and reverse translational strategies have revealed potential novel targets for CVD prevention in diabetes, including inhibition of apolipoprotein C3 (APOC3). Modeling and pharmacology-based approaches to improve insulin action provide additional potential strategies to combat CVD. The development of new strategies for improved diabetes and lipid control fuels hope for future prevention of CVD associated with diabetes.
MeSH term(s)	Animals ; Cardiovascular Diseases/etiology ; Cardiovascular Diseases/prevention & control ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/drug therapy ; Humans ; Hypoglycemic Agents/therapeutic use ; Insulin/therapeutic use ; Risk Factors
Chemical Substances	Hypoglycemic Agents ; Insulin
Language	English
Publishing date	2020-05-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2036490-8
ISSN	1471-499X ; 1471-4914
ISSN (online)	1471-499X
ISSN	1471-4914
DOI	10.1016/j.molmed.2020.03.011
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Article ; Online: A targeted proteomics method for quantifying plasma apolipoprotein kinetics in individual mice using stable isotope labeling.

Shao, Baohai / Shimizu-Albergine, Masami / Kramer, Farah / Kanter, Jenny E / Heinecke, Jay W / Vaisar, Tomas / Mittendorfer, Bettina / Patterson, Bruce W / Bornfeldt, Karin E

Journal of lipid research

2024 Volume 65, Issue 4, Page(s) 100531

Abstract: Altered apolipoprotein kinetics play a critical role in promoting dyslipidemia and atherogenesis. Human apolipoprotein kinetics have been extensively evaluated, but similar studies in mice are hampered by the lack of robust methods suitable for the small ...

Abstract	Altered apolipoprotein kinetics play a critical role in promoting dyslipidemia and atherogenesis. Human apolipoprotein kinetics have been extensively evaluated, but similar studies in mice are hampered by the lack of robust methods suitable for the small amounts of blood that can be collected at sequential time points from individual mice. We describe a targeted liquid chromatography tandem mass spectrometry method for simultaneously quantifying the stable isotope enrichment of several apolipoproteins represented by multiple peptides in serial blood samples (15 μl each) obtained after retro-orbital injection of
MeSH term(s)	Animals ; Mice ; Isotope Labeling ; Proteomics/methods ; Apolipoproteins/blood ; Kinetics ; Receptors, LDL/genetics ; Receptors, LDL/metabolism ; Apolipoproteins E/deficiency ; Apolipoproteins E/blood ; Chromatography, Liquid/methods ; Mice, Inbred C57BL ; Mice, Knockout ; Male
Chemical Substances	Apolipoproteins ; Receptors, LDL ; Apolipoproteins E
Language	English
Publishing date	2024-03-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80154-9
ISSN	1539-7262 ; 0022-2275
ISSN (online)	1539-7262
ISSN	0022-2275
DOI	10.1016/j.jlr.2024.100531
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Article: Monocytes and Macrophages as Protagonists in Vascular Complications of Diabetes.

Kanter, Jenny E / Hsu, Cheng-Chieh / Bornfeldt, Karin E

Frontiers in cardiovascular medicine

2020 Volume 7, Page(s) 10

Abstract: With the increasing prevalence of diabetes worldwide, vascular complications of diabetes are also on the rise. Diabetes results in an increased risk of macrovascular complications, with atherosclerotic cardiovascular disease (CVD) being the leading cause ...

Abstract	With the increasing prevalence of diabetes worldwide, vascular complications of diabetes are also on the rise. Diabetes results in an increased risk of macrovascular complications, with atherosclerotic cardiovascular disease (CVD) being the leading cause of death in adults with diabetes. The exact mechanisms for how diabetes promotes CVD risk are still unclear, although it is evident that monocytes and macrophages are key players in all stages of atherosclerosis both in the absence and presence of diabetes, and that phenotypes of these cells are altered by the diabetic environment. Evidence suggests that at least five pro-atherogenic mechanisms involving monocytes and macrophages contribute to the accelerated atherosclerotic lesion progression and hampered lesion regression associated with diabetes. These changes include (1) increased monocyte recruitment to lesions; (2) increased inflammatory activation; (3) altered macrophage lipid accumulation and metabolism; (4) increased macrophage cell death; and (5) reduced efferocytosis. Monocyte and macrophage phenotypes and mechanisms have been revealed mostly by different animal models of diabetes. The roles of specific changes in monocytes and macrophages in humans with diabetes remain largely unknown. There is an ongoing debate on whether the changes in monocytes and macrophages are caused by altered glucose levels, insulin deficiency or insulin resistance, lipid abnormalities, or combinations of these factors. Current research in humans and mouse models suggests that reduced clearance of triglyceride-rich lipoproteins and their remnants is one important mechanism whereby diabetes adversely affects macrophages and promotes atherosclerosis and CVD risk. Although monocytes and macrophages readily respond to the diabetic environment and can be seen as protagonists in diabetes-accelerated atherosclerosis, they are likely not instigators of the increased CVD risk.
Language	English
Publishing date	2020-02-14
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2781496-8
ISSN	2297-055X
ISSN	2297-055X
DOI	10.3389/fcvm.2020.00010
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Article ; Online: Hematopoietic NLRP3 and AIM2 Inflammasomes Promote Diabetes-Accelerated Atherosclerosis, but Increased Necrosis Is Independent of Pyroptosis.

Hsu, Cheng-Chieh / Fidler, Trevor P / Kanter, Jenny E / Kothari, Vishal / Kramer, Farah / Tang, Jingjing / Tall, Alan R / Bornfeldt, Karin E

Diabetes

2023 Volume 72, Issue 7, Page(s) 999–1011

Abstract: Serum apolipoprotein C3 (APOC3) predicts incident cardiovascular events in people with type 1 diabetes, and silencing of APOC3 prevents both lesion initiation and advanced lesion necrotic core expansion in a mouse model of type 1 diabetes. APOC3 acts by ... ...

Abstract	Serum apolipoprotein C3 (APOC3) predicts incident cardiovascular events in people with type 1 diabetes, and silencing of APOC3 prevents both lesion initiation and advanced lesion necrotic core expansion in a mouse model of type 1 diabetes. APOC3 acts by slowing the clearance of triglyceride-rich lipoproteins, but lipid-free APOC3 has recently been reported to activate an inflammasome pathway in monocytes. We therefore investigated the contribution of hematopoietic inflammasome pathways to atherosclerosis in mouse models of type 1 diabetes. LDL receptor-deficient diabetes mouse models were transplanted with bone marrow from donors deficient in NOD, LRR and pyrin domain-containing protein 3 (NLRP3), absent in melanoma 2 (AIM2) or gasdermin D (GSDMD), an inflammasome-induced executor of pyroptotic cell death. Mice with diabetes exhibited inflammasome activation and consistently, increased plasma interleukin-1β (IL-1β) and IL-18. Hematopoietic deletions of NLRP3, AIM2, or GSDMD caused smaller atherosclerotic lesions in diabetic mice. The increased lesion necrotic core size in diabetic mice was independent of macrophage pyroptosis because hematopoietic GSDMD deficiency failed to prevent necrotic core expansion in advanced lesions. Our findings demonstrate that AIM2 and NLRP3 inflammasomes contribute to atherogenesis in diabetes and suggest that necrotic core expansion is independent of macrophage pyroptosis. Article highlights: The contribution of hematopoietic cell inflammasome activation to atherosclerosis associated with type 1 diabetes is unknown. The goal of this study was to address whether hematopoietic NOD, LRR, and pyrin domain-containing protein 3 (NLRP3), absent in melanoma 2 (AIM2) inflammasomes, or the pyroptosis executioner gasdermin D (GSDMD) contributes to atherosclerosis in mouse models of type 1 diabetes. Diabetic mice exhibited increased inflammasome activation, with hematopoietic deletions of NLRP3, AIM2, or GSDMD causing smaller atherosclerotic lesions in diabetic mice, but the increased lesion necrotic core size in diabetic mice was independent of macrophage pyroptosis. Further studies on whether inflammasome activation contributes to cardiovascular complications in people with type 1 diabetes are warranted.
MeSH term(s)	Mice ; Animals ; Inflammasomes/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Pyroptosis/physiology ; Diabetes Mellitus, Type 1/complications ; Diabetes Mellitus, Experimental/complications ; Gasdermins ; Mice, Inbred NOD ; Atherosclerosis ; Necrosis ; Carrier Proteins ; Melanoma
Chemical Substances	Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Gasdermins ; Carrier Proteins
Language	English
Publishing date	2023-04-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db22-0962
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Article ; Online: Apolipoprotein C3 induces inflammasome activation only in its delipidated form.

Hsu, Cheng-Chieh / Shao, Baohai / Kanter, Jenny E / He, Yi / Vaisar, Tomas / Witztum, Joseph L / Snell-Bergeon, Janet / McInnes, Gregory / Bruse, Shannon / Gottesman, Omri / Mullick, Adam E / Bornfeldt, Karin E

Nature immunology

2023 Volume 24, Issue 3, Page(s) 408–411

MeSH term(s)	Apolipoprotein C-III ; Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein
Chemical Substances	Apolipoprotein C-III ; Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein
Language	English
Publishing date	2023-02-13
Publishing country	United States
Document type	Letter ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/s41590-023-01423-2
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