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Article ; Online: Gut check: assessing the role of the gut microbiota in the adverse cardiovascular effects of obstructive sleep apnoea.

Durgan, David J / Farré, Ramon

2023 Volume 61, Issue 1

MeSH term(s)	Humans ; Animals ; Mice ; Gastrointestinal Microbiome ; Disease Models, Animal ; Sleep Apnea, Obstructive/complications ; Sleep Apnea, Obstructive/physiopathology ; Sleep Apnea Syndromes ; Probiotics
Language	English
Publishing date	2023-01-19
Publishing country	England
Document type	Editorial ; Comment
ZDB-ID	639359-7
ISSN	1399-3003 ; 0903-1936
ISSN (online)	1399-3003
ISSN	0903-1936
DOI	10.1183/13993003.01974-2022
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Zs.A 2322: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Evidence for a gut-immune-vascular axis in the development of hypertension.

Durgan, David J

Acta physiologica (Oxford, England)

2019 Volume 227, Issue 1, Page(s) e13338

MeSH term(s)	Animals ; Blood Pressure ; Fecal Microbiota Transplantation ; Hypertension ; Immune System ; Rats
Language	English
Publishing date	2019-07-25
Publishing country	England
Document type	Editorial ; Comment
ZDB-ID	2218636-0
ISSN	1748-1716 ; 1748-1708
ISSN (online)	1748-1716
ISSN	1748-1708
DOI	10.1111/apha.13338
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Uc I Zs 229: Show issues

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Article ; Online: Obstructive Sleep Apnea-Induced Hypertension: Role of the Gut Microbiota.

Durgan, David J

Current hypertension reports

2017 Volume 19, Issue 4, Page(s) 35

Abstract: Purpose of review: Obstructive sleep apnea (OSA) is a significant risk factor for systemic hypertension and other cardiovascular diseases. While this relationship has been firmly established, a detailed understanding of how OSA leads to hypertension is ... ...

Abstract	Purpose of review: Obstructive sleep apnea (OSA) is a significant risk factor for systemic hypertension and other cardiovascular diseases. While this relationship has been firmly established, a detailed understanding of how OSA leads to hypertension is lacking. This review will examine the emerging idea that the gut microbiota plays a role in the development of hypertension, including that associated with OSA. Recent findings: Disruption of the normal composition of the gut microbiota, termed dysbiosis, has been identified in a number of metabolic and cardiovascular diseases, including diabetes, obesity, and atherosclerosis. Recently, a number of studies have demonstrated gut dysbiosis in various animal models of hypertension as well as in hypertensive patients. Evidence is now emerging that gut dysbiosis plays a causal role in the development of OSA-induced hypertension. In this review, we will examine the evidence that gut dysbiosis plays a role in OSA-induced hypertension. We will discuss potential mechanisms linking OSA to gut dysbiosis, examine how gut dysbiosis may be linked to hypertension, and highlight how this understanding may be utilized for the development of future therapeutics.
MeSH term(s)	Animals ; Dysbiosis ; Gastrointestinal Microbiome ; Humans ; Hypertension/microbiology ; Hypertension/physiopathology ; Obesity/complications ; Risk Factors ; Sleep Apnea, Obstructive/etiology
Language	English
Publishing date	2017-03-27
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2057367-4
ISSN	1534-3111 ; 1522-6417
ISSN (online)	1534-3111
ISSN	1522-6417
DOI	10.1007/s11906-017-0732-3
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Zs.A 5522: Show issues

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Article ; Online: Gut microbiota: a key regulator of ageing-associated atrial fibrillation?

Li, Na / Durgan, David J / Wehrens, Xander H T

Cardiovascular research

2021 Volume 118, Issue 3, Page(s) 657–659

MeSH term(s)	Aging ; Atrial Fibrillation/diagnosis ; Gastrointestinal Microbiome ; Humans
Language	English
Publishing date	2021-11-26
Publishing country	England
Document type	Editorial ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvab346
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Zs.A 565: Show issues

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Article ; Online: Obstructive Sleep Apnea-Induced Hypertension Is Associated With Increased Gut and Neuroinflammation.

Ayyaswamy, Sriram / Shi, Huanan / Zhang, Bojun / Bryan, Robert M / Durgan, David J

Journal of the American Heart Association

2023 Volume 12, Issue 11, Page(s) e029218

Abstract: Background Obstructive sleep apnea (OSA) is an independent risk factor for the development of hypertension. We have demonstrated that OSA induces gut dysbiosis, and this dysbiotic microbiota contributes to hypertension. However, the mechanisms linking ... ...

Abstract	Background Obstructive sleep apnea (OSA) is an independent risk factor for the development of hypertension. We have demonstrated that OSA induces gut dysbiosis, and this dysbiotic microbiota contributes to hypertension. However, the mechanisms linking gut dysbiosis to blood pressure regulation remain unclear. Recent studies demonstrate that gut dysbiosis can induce a proinflammatory response of the host resulting in peripheral and neuroinflammation, key factors in the development of hypertension. We hypothesized that OSA induces inflammation in the gut that contributes to neuroinflammation and hypertension. Methods and Results OSA was induced in 8-week-old male rats. After 2 weeks of apneas, lymphocytes were isolated from aorta, brain, cecum, ileum, mesenteric lymph node, and spleen for flow cytometry. To examine the role of interleukin-17a, a monoclonal antibody was administered to neutralize interleukin-17a. Lymphocytes originating from the gut were tracked by labeling with carboxyfluorescein succinimidyl ester dye. OSA led to a significant decrease in T regulatory cells along with an increase in T helper (T
MeSH term(s)	Rats ; Male ; Animals ; Interleukin-17 ; Neuroinflammatory Diseases ; Dysbiosis/complications ; Gastrointestinal Microbiome/physiology ; Sleep Apnea, Obstructive/complications ; Hypertension
Chemical Substances	Interleukin-17
Language	English
Publishing date	2023-06-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2653953-6
ISSN	2047-9980 ; 2047-9980
ISSN (online)	2047-9980
ISSN	2047-9980
DOI	10.1161/JAHA.122.029218
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Article ; Online: Lysosome damage triggers direct ATG8 conjugation and ATG2 engagement via non-canonical autophagy.

Cross, Jake / Durgan, Joanne / McEwan, David G / Tayler, Matthew / Ryan, Kevin M / Florey, Oliver

The Journal of cell biology

2023 Volume 222, Issue 12

Abstract: Cells harness multiple pathways to maintain lysosome integrity, a central homeostatic process. Damaged lysosomes can be repaired or targeted for degradation by lysophagy, a selective autophagy process involving ATG8/LC3. Here, we describe a parallel ATG8/ ...

Abstract	Cells harness multiple pathways to maintain lysosome integrity, a central homeostatic process. Damaged lysosomes can be repaired or targeted for degradation by lysophagy, a selective autophagy process involving ATG8/LC3. Here, we describe a parallel ATG8/LC3 response to lysosome damage, mechanistically distinct from lysophagy. Using a comprehensive series of biochemical, pharmacological, and genetic approaches, we show that lysosome damage induces non-canonical autophagy and Conjugation of ATG8s to Single Membranes (CASM). Following damage, ATG8s are rapidly and directly conjugated onto lysosome membranes, independently of ATG13/WIPI2, lipidating to PS (and PE), a molecular hallmark of CASM. Lysosome damage drives V-ATPase V0-V1 association, direct recruitment of ATG16L1 via its WD40-domain/K490A, and is sensitive to Salmonella SopF. Lysosome damage-induced CASM is associated with formation of dynamic, LC3A-positive tubules, and promotes robust LC3A engagement with ATG2, a lipid transfer protein central to lysosome repair. Together, our data identify direct ATG8 conjugation as a rapid response to lysosome damage, with important links to lipid transfer and dynamics.
MeSH term(s)	Autophagy/genetics ; Lysosomes/genetics ; Lysosomes/metabolism ; Macroautophagy/genetics ; Microtubule-Associated Proteins/metabolism ; Salmonella ; Autophagy-Related Protein 8 Family/genetics ; Autophagy-Related Protein 8 Family/metabolism
Chemical Substances	Microtubule-Associated Proteins ; Autophagy-Related Protein 8 Family
Language	English
Publishing date	2023-10-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218154-x
ISSN	1540-8140 ; 0021-9525
ISSN (online)	1540-8140
ISSN	0021-9525
DOI	10.1083/jcb.202303078
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Article ; Online: Alterations of the gut microbial community structure and function with aging in the spontaneously hypertensive stroke prone rat.

Shi, Huanan / Nelson, James W / Phillips, Sharon / Petrosino, Joseph F / Bryan, Robert M / Durgan, David J

Scientific reports

2022 Volume 12, Issue 1, Page(s) 8534

Abstract: Gut dysbiosis, a pathological imbalance of bacteria, has been shown to contribute to the development of hypertension (HT), systemic- and neuro-inflammation, and blood-brain barrier (BBB) disruption in spontaneously hypertensive stroke prone rats (SHRSP). ...

Abstract	Gut dysbiosis, a pathological imbalance of bacteria, has been shown to contribute to the development of hypertension (HT), systemic- and neuro-inflammation, and blood-brain barrier (BBB) disruption in spontaneously hypertensive stroke prone rats (SHRSP). However, to date individual species that contribute to HT in the SHRSP model have not been identified. One potential reason, is that nearly all studies of the SHRSP gut microbiota have analyzed samples from rats with established HT. The goal of this study was to examine the SHRSP gut microbiota before, during, and after the onset of hypertension, and in normotensive WKY control rats over the same age range. We hypothesized that we could identify key microbes involved in the development of HT by comparing WKY and SHRSP microbiota during the pre-hypertensive state and longitudinally. Systolic blood pressure (SBP) was measured by tail-cuff plethysmography and fecal microbiota analyzed by16S rRNA gene sequencing. SHRSP showed significant elevations in SBP, as compared to WKY, beginning at 8 weeks of age (p < 0.05 at each time point). Bacterial community structure was significantly different between WKY and SHRSP as early as 4 weeks of age, and remained different throughout the study (p = 0.001-0.01). At the phylum level we observed significantly reduced Firmicutes and Deferribacterota, and elevated Bacteroidota, Verrucomicrobiota, and Proteobacteria, in pre-hypertensive SHRSP, as compared to WKY. At the genus level we identified 18 bacteria whose relative abundance was significantly different in SHRSP versus WKY at the pre-hypertensive ages of 4 or 6 weeks. In an attempt to further refine bacterial candidates that might contribute to the SHRSP phenotype, we compared the functional capacity of WKY versus SHRSP microbial communities. We identified significant differences in amino acid metabolism. Using untargeted metabolomics we found significant reductions in metabolites of the tryptophan-kynurenine pathway and increased indole metabolites in SHRSP versus WKY plasma. Overall, we provide further evidence that gut dysbiosis contributes to hypertension in the SHRSP model, and suggest for the first time the potential involvement of tryptophan metabolizing microbes.
MeSH term(s)	Aging ; Animals ; Blood Pressure/physiology ; Dysbiosis ; Gastrointestinal Microbiome ; Hypertension ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Stroke ; Tryptophan
Chemical Substances	Tryptophan (8DUH1N11BX)
Language	English
Publishing date	2022-05-20
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-12578-7
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Article ; Online: Prospects for Leveraging the Microbiota as Medicine for Hypertension.

Durgan, David J / Zubcevic, Jasenka / Vijay-Kumar, Matam / Yang, Tao / Manandhar, Ishan / Aryal, Sachin / Muralitharan, Rikeish R / Li, Hong-Bao / Li, Ying / Abais-Battad, Justine M / Pluznick, Jennifer L / Muller, Dominik N / Marques, Francine Z / Joe, Bina

Hypertension (Dallas, Tex. : 1979)

2024 Volume 81, Issue 5, Page(s) 951–963

MeSH term(s)	Humans ; Hypertension ; Blood Pressure ; Microbiota
Language	English
Publishing date	2024-04-17
Publishing country	United States
Document type	Journal Article ; 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.124.21721
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Zs.A 1488: Show issues

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Article ; Online: Combating hypertension beyond genome-wide association studies: Microbiome and artificial intelligence as opportunities for precision medicine.

Aryal, Sachin / Manandhar, Ishan / Mei, Xue / Yeoh, Beng S / Tummala, Ramakumar / Saha, Piu / Osman, Islam / Zubcevic, Jasenka / Durgan, David J / Vijay-Kumar, Matam / Joe, Bina

Cambridge prisms. Precision medicine

2023 Volume 1, Page(s) e26

Abstract: The single largest contributor to human mortality is cardiovascular disease, the top risk factor for which is hypertension (HTN). The last two decades have placed much emphasis on the identification of genetic factors contributing to HTN. As a result, ... ...

Abstract	The single largest contributor to human mortality is cardiovascular disease, the top risk factor for which is hypertension (HTN). The last two decades have placed much emphasis on the identification of genetic factors contributing to HTN. As a result, over 1,500 genetic alleles have been associated with human HTN. Mapping studies using genetic models of HTN have yielded hundreds of blood pressure (BP) loci but their individual effects on BP are minor, which limits opportunities to target them in the clinic. The value of collecting genome-wide association data is evident in ongoing research, which is beginning to utilize these data at individual-level genetic disparities combined with artificial intelligence (AI) strategies to develop a polygenic risk score (PRS) for the prediction of HTN. However, PRS alone may or may not be sufficient to account for the incidence and progression of HTN because genetics is responsible for <30% of the risk factors influencing the etiology of HTN pathogenesis. Therefore, integrating data from other nongenetic factors influencing BP regulation will be important to enhance the power of PRS. One such factor is the composition of gut microbiota, which constitute a more recently discovered important contributor to HTN. Studies to-date have clearly demonstrated that the transition from normal BP homeostasis to a state of elevated BP is linked to compositional changes in gut microbiota and its interaction with the host. Here, we first document evidence from studies on gut dysbiosis in animal models and patients with HTN followed by a discussion on the prospects of using microbiota data to develop a metagenomic risk score (MRS) for HTN to be combined with PRS and a clinical risk score (CRS). Finally, we propose that integrating AI to learn from the combined PRS, MRS and CRS may further enhance predictive power for the susceptibility and progression of HTN.
Language	English
Publishing date	2023-05-16
Publishing country	England
Document type	Journal Article ; Review
ISSN	2752-6143
ISSN (online)	2752-6143
DOI	10.1017/pcm.2023.13
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Article ; Online: The rat cerebral vasculature exhibits time-of-day-dependent oscillations in circadian clock genes and vascular function that are attenuated following obstructive sleep apnea.

Durgan, David J / Crossland, Randy F / Bryan, Robert M

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism

2017 Volume 37, Issue 8, Page(s) 2806–2819

Abstract: Circadian clock components oscillate in cells of the cardiovascular system. Disruption of these oscillations has been observed in cardiovascular diseases. We hypothesized that obstructive sleep apnea, which is associated with cerebrovascular diseases, ... ...

Abstract	Circadian clock components oscillate in cells of the cardiovascular system. Disruption of these oscillations has been observed in cardiovascular diseases. We hypothesized that obstructive sleep apnea, which is associated with cerebrovascular diseases, disrupts the cerebrovascular circadian clock and rhythms in vascular function. Apneas were produced in rats during sleep. Following two weeks of sham or obstructive sleep apnea, cerebral arteries were isolated over 24 h for mRNA and functional analysis. mRNA expression of clock genes exhibited 24-h rhythms in cerebral arteries of sham rats (p < 0.05). Interestingly, peak expression of clock genes was significantly lower following obstructive sleep apnea (p < 0.05). Obstructive sleep apnea did not alter clock genes in the heart, or rhythms in locomotor activity. Isolated posterior cerebral arteries from sham rats exhibited a diurnal rhythm in sensitivity to luminally applied ATP, being most responsive at the beginning of the active phase (p < 0.05). This rhythm was absent in arteries from obstructive sleep apnea rats (p < 0.05). Rhythms in ATP sensitivity in sham vessels were absent, and not different from obstructive sleep apnea, following treatment with L-NAME and indomethacin. We conclude that cerebral arteries possess a functional circadian clock and exhibit a diurnal rhythm in vasoreactivity to ATP. Obstructive sleep apnea attenuates these rhythms in cerebral arteries, potentially contributing to obstructive sleep apnea-associated cerebrovascular disease.
MeSH term(s)	Animals ; Cerebral Arteries/physiopathology ; Cerebrovascular Disorders/etiology ; Cerebrovascular Disorders/genetics ; Cerebrovascular Disorders/physiopathology ; Circadian Clocks/genetics ; Circadian Clocks/physiology ; Circadian Rhythm/genetics ; Circadian Rhythm/physiology ; Disease Models, Animal ; Period Circadian Proteins/genetics ; Rats, Long-Evans ; Sleep Apnea, Obstructive/complications ; Sleep Apnea, Obstructive/genetics ; Sleep Apnea, Obstructive/physiopathology ; Vasodilation/physiology
Chemical Substances	Period Circadian Proteins
Language	English
Publishing date	2017-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	604628-9
ISSN	1559-7016 ; 0271-678X
ISSN (online)	1559-7016
ISSN	0271-678X
DOI	10.1177/0271678X16675879
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