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Article ; Online: Empagliflozin Reverses Oxidized LDL-Induced RECK Suppression, Cardiotrophin-1 Expression, MMP Activation, and Human Aortic Smooth Muscle Cell Proliferation and Migration.

Chandrasekar, Bysani / Mummidi, Srinivas / DeMarco, Vincent G / Higashi, Yusuke

2023 Volume 2023, Page(s) 6112301

Abstract: Persistent oxidative stress and inflammation contribute causally to smooth muscle cell (SMC) proliferation and migration, the characteristic features of vascular proliferative diseases. Oxidatively modified low-density lipoproteins (OxLDL) elevate ... ...

Abstract	Persistent oxidative stress and inflammation contribute causally to smooth muscle cell (SMC) proliferation and migration, the characteristic features of vascular proliferative diseases. Oxidatively modified low-density lipoproteins (OxLDL) elevate oxidative stress levels, inflammatory responses, and matrix metallopeptidase (MMP) activation, resulting ultimately in SMC migration, proliferation, and phenotype change. Reversion-inducing cysteine-rich protein with Kazal motifs (RECK) is a membrane-anchored MMP inhibitor. Empagliflozin is an SGLT2 inhibitor and exerts pleiotropic cardiovascular protective effects, including antioxidant and anti-inflammatory effects. Here, we investigated (i) whether OxLDL regulates RECK expression, (ii) whether ectopic expression of RECK reverses OxLDL-induced SMC migration and proliferation, and (iii) whether pretreatment with empagliflozin reverses OxLDL-induced RECK suppression, MMP activation, and SMC migration, proliferation, and differentiation. Indeed, results show that OxLDL at pathophysiological concentration promotes SMC migration and proliferation via NF-
MeSH term(s)	Humans ; Cytokine Receptor gp130 ; Lipoproteins, LDL/pharmacology ; Cell Proliferation ; MicroRNAs/metabolism ; Muscle, Smooth/metabolism ; GPI-Linked Proteins/metabolism
Chemical Substances	oxidized low density lipoprotein ; empagliflozin (HDC1R2M35U) ; Cytokine Receptor gp130 (133483-10-0) ; Lipoproteins, LDL ; MicroRNAs ; GPI-Linked Proteins ; RECK protein, human
Language	English
Publishing date	2023-10-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	1137605-3
ISSN	1466-1861 ; 0962-9351
ISSN (online)	1466-1861
ISSN	0962-9351
DOI	10.1155/2023/6112301
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Zs.A 3575: Show issues

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Article ; Online: Abstinence Restores Cardiac Function in Mice with Established Alcohol-Induced Cardiomyopathy.

Edavettal, Joshua M / Harris, Nicholas R / Cohen, Sarah E / Paloczi, Janos / Chandrasekar, Bysani / Gardner, Jason D

Cells

2023 Volume 12, Issue 24

Abstract: Alcohol-induced cardiomyopathy (ACM) has a poor prognosis with up to a 50% chance of death within four years of diagnosis. There are limited studies investigating the potential of abstinence for promoting repair after alcohol-induced cardiac damage, ... ...

Abstract	Alcohol-induced cardiomyopathy (ACM) has a poor prognosis with up to a 50% chance of death within four years of diagnosis. There are limited studies investigating the potential of abstinence for promoting repair after alcohol-induced cardiac damage, particularly in a controlled preclinical study design. Here, we developed an exposure protocol that led to significant decreases in cardiac function in C57BL6/J mice within 30 days; dP/dt max decreased in the mice fed alcohol for 30 days (8054 ± 664.5 mmHg/s compared to control mice: 11,188 ± 724.2 mmHg/s,
MeSH term(s)	Mice ; Animals ; Heart ; Cardiomyopathies/etiology ; Blood Pressure ; Ethanol/adverse effects ; Biomarkers
Chemical Substances	Ethanol (3K9958V90M) ; Biomarkers
Language	English
Publishing date	2023-12-07
Publishing country	Switzerland
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12242783
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Article ; Online: Integrated miRNA-mRNA networks underlie attenuation of chronic β-adrenergic stimulation-induced cardiac remodeling by minocycline.

Russell, Jacob J / Mummidi, Srinivas / DeMarco, Vincent G / Grisanti, Laurel A / Bailey, Chastidy A / Bender, Shawn B / Chandrasekar, Bysani

Physiological genomics

2024 Volume 56, Issue 4, Page(s) 360–366

Abstract: Adverse cardiac remodeling contributes to heart failure development and progression, partly due to inappropriate sympathetic nervous system activation. Although β-adrenergic receptor (β-AR) blockade is a common heart failure therapy, not all patients ... ...

Abstract	Adverse cardiac remodeling contributes to heart failure development and progression, partly due to inappropriate sympathetic nervous system activation. Although β-adrenergic receptor (β-AR) blockade is a common heart failure therapy, not all patients respond, prompting exploration of alternative treatments. Minocycline, an FDA-approved antibiotic, has pleiotropic properties beyond antimicrobial action. Recent evidence suggests it may alter gene expression via changes in miRNA expression. Thus, we hypothesized that minocycline could prevent adverse cardiac remodeling induced by the β-AR agonist isoproterenol, involving miRNA-mRNA transcriptome alterations. Male C57BL/6J mice received isoproterenol (30 mg/kg/day sc) or vehicle via osmotic minipump for 21 days, along with daily minocycline (50 mg/kg ip) or sterile saline. Isoproterenol induced cardiac hypertrophy without altering cardiac function, which minocycline prevented. Total mRNA sequencing revealed isoproterenol altering gene networks associated with inflammation and metabolism, with fibrosis activation predicted by integrated miRNA-mRNA sequencing, involving miR-21, miR-30a, miR-34a, miR-92a, and miR-150, among others. Conversely, the cardiac miRNA-mRNA transcriptome predicted fibrosis inhibition in minocycline-treated mice, involving antifibrotic shifts in Atf3 and Itgb6 gene expression associated with miR-194 upregulation. Picrosirius red staining confirmed isoproterenol-induced cardiac fibrosis, prevented by minocycline. These results demonstrate minocycline's therapeutic potential in attenuating adverse cardiac remodeling through miRNA-mRNA-dependent mechanisms, especially in reducing cardiac fibrosis.
MeSH term(s)	Humans ; Male ; Mice ; Animals ; Isoproterenol/pharmacology ; Isoproterenol/metabolism ; Minocycline/pharmacology ; Myocytes, Cardiac/metabolism ; Adrenergic Agents/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; RNA, Messenger/genetics ; Ventricular Remodeling/genetics ; Mice, Inbred C57BL ; Cardiomegaly/metabolism ; Cardiomyopathies ; Heart Failure/chemically induced ; Heart Failure/drug therapy ; Heart Failure/genetics ; Fibrosis
Chemical Substances	Isoproterenol (L628TT009W) ; Minocycline (FYY3R43WGO) ; Adrenergic Agents ; MicroRNAs ; RNA, Messenger
Language	English
Publishing date	2024-02-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	2038823-8
ISSN	1531-2267 ; 1094-8341
ISSN (online)	1531-2267
ISSN	1094-8341
DOI	10.1152/physiolgenomics.00140.2023
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Zs.A 5697: Show issues

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Article: The Role of RECK in Hepatobiliary Neoplasia Reveals Its Therapeutic Potential in NASH.

Dashek, Ryan J / Diaz, Connor / Chandrasekar, Bysani / Rector, R Scott

Frontiers in endocrinology

2021 Volume 12, Page(s) 770740

Abstract: Non-alcoholic fatty liver disease (NAFLD) is a multimorbidity disorder ranging from excess accumulation of fat in the liver (steatosis) to steatohepatitis (NASH) and end-stage cirrhosis, and the development of hepatocellular carcinoma (HCC) in a subset ... ...

Abstract	Non-alcoholic fatty liver disease (NAFLD) is a multimorbidity disorder ranging from excess accumulation of fat in the liver (steatosis) to steatohepatitis (NASH) and end-stage cirrhosis, and the development of hepatocellular carcinoma (HCC) in a subset of patients. The defining features of NASH are inflammation and progressive fibrosis. Currently, no pharmaceutical therapies are available for NAFLD, NASH and HCC; therefore, developing novel treatment strategies is desperately needed. Reversion Inducing Cysteine Rich Protein with Kazal motifs (RECK) is a well-known modifier of the extracellular matrix in hepatic remodeling and transition to HCC. More recently, its role in regulating inflammatory and fibrogenic processes has emerged. Here, we summarize the most relevant findings that extend our current understanding of RECK as a regulator of inflammation and fibrosis, and its induction as a potential strategy to blunt the development and progression of NASH and HCC.
MeSH term(s)	Bile Duct Neoplasms/genetics ; Bile Duct Neoplasms/metabolism ; Bile Duct Neoplasms/pathology ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/pathology ; GPI-Linked Proteins/genetics ; GPI-Linked Proteins/metabolism ; Humans ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Liver Neoplasms/pathology ; Non-alcoholic Fatty Liver Disease/genetics ; Non-alcoholic Fatty Liver Disease/metabolism ; Non-alcoholic Fatty Liver Disease/pathology
Chemical Substances	GPI-Linked Proteins ; RECK protein, human
Language	English
Publishing date	2021-10-20
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2021.770740
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Article ; Online: Quantification of myocardial fibrosis using noninvasive T2-mapping magnetic resonance imaging: Preclinical models of aging and pressure overload.

Lee, Li E / Chandrasekar, Bysani / Yu, Ping / Ma, Lixin

NMR in biomedicine

2021 Volume 35, Issue 3, Page(s) e4641

Abstract: Noninvasive imaging of cardiac fibrosis is important for early diagnosis and intervention in chronic heart diseases. Here, we investigated whether noninvasive, contrast agent-free MRI ... ...

Abstract	Noninvasive imaging of cardiac fibrosis is important for early diagnosis and intervention in chronic heart diseases. Here, we investigated whether noninvasive, contrast agent-free MRI T
MeSH term(s)	Aging/pathology ; Aging/physiology ; Animals ; Cardiomegaly/diagnostic imaging ; Diastole/physiology ; Fibrosis/diagnostic imaging ; Magnetic Resonance Imaging/methods ; Male ; Mice ; Mice, Inbred C57BL ; Myocardium/pathology
Language	English
Publishing date	2021-11-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1000976-0
ISSN	1099-1492 ; 0952-3480
ISSN (online)	1099-1492
ISSN	0952-3480
DOI	10.1002/nbm.4641
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Zs.A 2869: Show issues

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Article ; Online: Unfolded protein response and angiogenesis in malignancies.

Izadpanah, Amin / Willingham, Kurtis / Chandrasekar, Bysani / Alt, Eckhard U / Izadpanah, Reza

Biochimica et biophysica acta. Reviews on cancer

2022 Volume 1878, Issue 2, Page(s) 188839

Abstract: Cellular stress, arising from accumulation of unfolded proteins, occurs frequently in rapidly proliferating cancer cells. This cellular stress, in turn, activates the unfolded protein response (UPR), an interconnected set of signal transduction pathways ... ...

Abstract	Cellular stress, arising from accumulation of unfolded proteins, occurs frequently in rapidly proliferating cancer cells. This cellular stress, in turn, activates the unfolded protein response (UPR), an interconnected set of signal transduction pathways that alleviate the proteostatic stress. The UPR is implicated in cancer cell survival and proliferation through upregulation of pro-tumorigenic pathways that ultimately promote malignant metabolism and neoangiogenesis. Here, we reviewed mechanisms of signaling crosstalk between the UPR and angiogenesis pathways, as well as transmissible ER stress and the role in tumor growth and development. To characterize differences in UPR and UPR-mediated angiogenesis in malignancy, we employed a data mining approach using patient tumor data from The Cancer Genome Atlas (TCGA). The analysis of TCGA revealed differences in UPR between malignant samples versus their non-malignant counterparts.
MeSH term(s)	Humans ; Unfolded Protein Response ; Signal Transduction/genetics ; Neoplasms ; Transcriptional Activation ; Neovascularization, Pathologic
Language	English
Publishing date	2022-11-19
Publishing country	Netherlands
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2918802-7
ISSN	1879-2561 ; 0304-419X
ISSN (online)	1879-2561
ISSN	0304-419X
DOI	10.1016/j.bbcan.2022.188839
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Zs.A 7162: Show issues

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Article ; Online: Macrophage-Specific IGF-1 Overexpression Reduces CXCL12 Chemokine Levels and Suppresses Atherosclerotic Burden in Apoe-Deficient Mice.

Snarski, Patricia / Sukhanov, Sergiy / Yoshida, Tadashi / Higashi, Yusuke / Danchuk, Svitlana / Chandrasekar, Bysani / Tian, Di / Rivera-Lopez, Vikara / Delafontaine, Patrick

Arteriosclerosis, thrombosis, and vascular biology

2021 Volume 42, Issue 2, Page(s) 113–126

Abstract: Objective: IGF-1 (insulin-like growth factor 1) exerts pleiotropic effects including promotion of cellular growth, differentiation, survival, and anabolism. We have shown that systemic IGF-1 administration reduced atherosclerosis in Apoe: Conclusions!# ...

Abstract	Objective: IGF-1 (insulin-like growth factor 1) exerts pleiotropic effects including promotion of cellular growth, differentiation, survival, and anabolism. We have shown that systemic IGF-1 administration reduced atherosclerosis in Apoe Conclusions: Macrophage IGF-1 overexpression reduced atherosclerotic burden and increased features of plaque stability, likely via a reduction in CXCL12-mediated monocyte recruitment and an increase in ABCA1-dependent macrophage lipid efflux.
MeSH term(s)	Animals ; Apolipoproteins E/genetics ; Atherosclerosis/blood ; Atherosclerosis/genetics ; Atherosclerosis/pathology ; Chemokine CXCL12/analysis ; Chemokine CXCL12/blood ; Female ; Gene Deletion ; Humans ; Insulin-Like Growth Factor I/genetics ; Macrophages/metabolism ; Male ; Mice ; Mice, Knockout ; Rats ; THP-1 Cells ; Up-Regulation
Chemical Substances	Apolipoproteins E ; Chemokine CXCL12 ; Cxcl12 protein, mouse ; insulin-like growth factor-1, rat ; Insulin-Like Growth Factor I (67763-96-6)
Language	English
Publishing date	2021-12-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.121.316090
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Zs.A 1705: Show issues

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Article ; Online: Aldosterone impairs coronary adenosine-mediated vasodilation via reduced functional expression of Ca

Khan, Maloree / Meuth, Alex I / Brown, Scott M / Chandrasekar, Bysani / Bowles, Douglas K / Bender, Shawn B

American journal of physiology. Heart and circulatory physiology

2019 Volume 317, Issue 2, Page(s) H357–H363

Abstract: Elevated plasma aldosterone (Aldo) levels are associated with greater risk of cardiac ischemic events and cardiovascular mortality. Adenosine-mediated coronary vasodilation is a critical cardioprotective mechanism during ischemia; however, whether this ... ...

Abstract	Elevated plasma aldosterone (Aldo) levels are associated with greater risk of cardiac ischemic events and cardiovascular mortality. Adenosine-mediated coronary vasodilation is a critical cardioprotective mechanism during ischemia; however, whether this response is impaired by increased Aldo is unclear. We hypothesized that chronic Aldo impairs coronary adenosine-mediated vasodilation via downregulation of vascular K
MeSH term(s)	Adenosine/pharmacology ; Aldosterone/pharmacology ; Animals ; Coronary Vessels/drug effects ; Coronary Vessels/metabolism ; Cyclic AMP/metabolism ; Down-Regulation ; Male ; Mice, Inbred C57BL ; Potassium Channels, Calcium-Activated/drug effects ; Potassium Channels, Calcium-Activated/genetics ; Potassium Channels, Calcium-Activated/metabolism ; Receptor, Adenosine A2A/genetics ; Receptor, Adenosine A2A/metabolism ; Signal Transduction ; Vasodilation/drug effects ; Vasodilator Agents/pharmacology
Chemical Substances	Adora2a protein, mouse ; Potassium Channels, Calcium-Activated ; Receptor, Adenosine A2A ; Vasodilator Agents ; Aldosterone (4964P6T9RB) ; Cyclic AMP (E0399OZS9N) ; Adenosine (K72T3FS567)
Language	English
Publishing date	2019-06-14
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.
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00081.2019
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Article ; Online: Minocycline inhibits PDGF-BB-induced human aortic smooth muscle cell proliferation and migration by reversing miR-221- and -222-mediated RECK suppression.

Higashi, Yusuke / Mummidi, Srinivas / Sukhanov, Sergiy / Yoshida, Tadashi / Noda, Makoto / Delafontaine, Patrice / Chandrasekar, Bysani

Cellular signalling

2019 Volume 57, Page(s) 10–20

Abstract: Minocycline, a tetracycline antibiotic, is known to exert vasculoprotective effects independent of its anti-bacterial properties; however the underlying molecular mechanisms are not completely understood. Reversion Inducing Cysteine Rich Protein with ... ...

Abstract	Minocycline, a tetracycline antibiotic, is known to exert vasculoprotective effects independent of its anti-bacterial properties; however the underlying molecular mechanisms are not completely understood. Reversion Inducing Cysteine Rich Protein with Kazal Motifs (RECK) is a cell surface expressed, membrane anchored protein, and its overexpression inhibits cancer cell migration. We hypothesized that minocycline inhibits platelet-derived growth factor (PDGF)-induced human aortic smooth muscle cell (SMC) proliferation and migration via RECK upregulation. Our data show that the BB homodimer of recombinant PDGF (PDGF-BB) induced SMC migration and proliferation, effects significantly blunted by pre-treatment with minocycline. Further investigations revealed that PDGF-BB induced PI3K-dependent AKT activation, ERK activation, reactive oxygen species generation, Nuclear Factor-κB and Activator Protein-1 activation, microRNA (miR)-221 and miR-222 induction, RECK suppression, and matrix metalloproteinase (MMP2 and 9) activation, effects that were reversed by minocycline. Notably, minocycline induced RECK expression dose-dependently within the therapeutic dose of 1-100 μM, and silencing RECK partially reversed the inhibitory effects of minocycline on PDGF-BB-induced MMP activation, and SMC proliferation and migration. Further, targeting MMP2 and MMP9 blunted PDGF-BB-induced SMC migration. Together, these results demonstrate that minocycline inhibits PDGF-BB-induced SMC proliferation and migration by restoring RECK, an MMP inhibitor. These results indicate that the induction of RECK is one of the mechanisms by which minocycline exerts vasculoprotective effects.
MeSH term(s)	Cell Movement/drug effects ; Cell Proliferation/drug effects ; GPI-Linked Proteins/drug effects ; GPI-Linked Proteins/genetics ; Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Minocycline/pharmacology ; Muscle, Smooth, Vascular/drug effects ; Muscle, Smooth, Vascular/metabolism ; Myocytes, Smooth Muscle/drug effects ; Myocytes, Smooth Muscle/metabolism ; Phosphatidylinositol 3-Kinases/drug effects ; Phosphatidylinositol 3-Kinases/metabolism
Chemical Substances	GPI-Linked Proteins ; MIRN221 microRNA, human ; MIRN222 microRNA, human ; MicroRNAs ; RECK protein, human ; Minocycline (FYY3R43WGO)
Language	English
Publishing date	2019-02-01
Publishing country	England
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.
ZDB-ID	1002702-6
ISSN	1873-3913 ; 0898-6568
ISSN (online)	1873-3913
ISSN	0898-6568
DOI	10.1016/j.cellsig.2019.01.014
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Zs.A 2579: Show issues

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Article ; Online: Multi-omic analysis of the cardiac cellulome defines a vascular contribution to cardiac diastolic dysfunction in obese female mice.

Dona, Malathi S I / Hsu, Ian / Meuth, Alex I / Brown, Scott M / Bailey, Chastidy A / Aragonez, Christian G / Russell, Jacob J / Krstevski, Crisdion / Aroor, Annayya R / Chandrasekar, Bysani / Martinez-Lemus, Luis A / DeMarco, Vincent G / Grisanti, Laurel A / Jaffe, Iris Z / Pinto, Alexander R / Bender, Shawn B

Basic research in cardiology

2023 Volume 118, Issue 1, Page(s) 11

Abstract: Coronary microvascular dysfunction (CMD) is associated with cardiac dysfunction and predictive of cardiac mortality in obesity, especially in females. Clinical data further support that CMD associates with development of heart failure with preserved ... ...

Abstract	Coronary microvascular dysfunction (CMD) is associated with cardiac dysfunction and predictive of cardiac mortality in obesity, especially in females. Clinical data further support that CMD associates with development of heart failure with preserved ejection fraction and that mineralocorticoid receptor (MR) antagonism may be more efficacious in obese female, versus male, HFpEF patients. Accordingly, we examined the impact of smooth muscle cell (SMC)-specific MR deletion on obesity-associated coronary and cardiac diastolic dysfunction in female mice. Obesity was induced in female mice via western diet (WD) feeding alongside littermates fed standard diet. Global MR blockade with spironolactone prevented coronary and cardiac dysfunction in obese females and specific deletion of SMC-MR was sufficient to prevent obesity-associated coronary and cardiac diastolic dysfunction. Cardiac gene expression profiling suggested reduced cardiac inflammation in WD-fed mice with SMC-MR deletion independent of blood pressure, aortic stiffening, and cardiac hypertrophy. Further mechanistic studies utilizing single-cell RNA sequencing of non-cardiomyocyte cell populations revealed novel impacts of SMC-MR deletion on the cardiac cellulome in obese mice. Specifically, WD feeding induced inflammatory gene signatures in non-myocyte populations including B/T cells, macrophages, and endothelium as well as increased coronary VCAM-1 protein expression, independent of cardiac fibrosis, that was prevented by SMC-MR deletion. Further, SMC-MR deletion induced a basal reduction in cardiac mast cells and prevented WD-induced cardiac pro-inflammatory chemokine expression and leukocyte recruitment. These data reveal a central role for SMC-MR signaling in obesity-associated coronary and cardiac dysfunction, thus supporting the emerging paradigm of a vascular origin of cardiac dysfunction in obesity.
MeSH term(s)	Male ; Female ; Mice ; Animals ; Mice, Obese ; Heart Failure/complications ; Multiomics ; Receptors, Mineralocorticoid/genetics ; Receptors, Mineralocorticoid/metabolism ; Stroke Volume ; Cardiomyopathies ; Mineralocorticoid Receptor Antagonists/pharmacology ; Obesity/metabolism
Chemical Substances	Receptors, Mineralocorticoid ; Mineralocorticoid Receptor Antagonists
Language	English
Publishing date	2023-03-29
Publishing country	Germany
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	189755-x
ISSN	1435-1803 ; 0300-8428 ; 0175-9418
ISSN (online)	1435-1803
ISSN	0300-8428 ; 0175-9418
DOI	10.1007/s00395-023-00983-6
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