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  1. AU="Inna P. Gladysheva"
  2. AU="Maeder, Claudia"
  3. AU="Delisle, Éolie"
  4. AU="Loïc Tetrel"
  5. AU="Kanske, Philipp"
  6. AU=Wu Chuang
  7. AU="John Alake"
  8. AU="McCarty, John M"
  9. AU="Rieger, Dirk"
  10. AU="Maria Camilla Cipriani"
  11. AU="Yu, Mo-Sang"
  12. AU="Arshad, Hassaan Bin"
  13. AU="Schwänke, Ulf"
  14. AU=Martin Rick
  15. AU="Narges ROUSTAEI"
  16. AU="Alsaady, Ammar"
  17. AU=Guo Zhinian
  18. AU=Dho Sascha E
  19. AU="Santiso-Quiñones, Gustavo"
  20. AU="Donovan, Lois E"
  21. AU="Xiong, Zhuo-Chao"
  22. AU="Mu, Dezhi"
  23. AU="Kaiser, Steffen"
  24. AU=Garlepp M J
  25. AU=Yang Zhenwei
  26. AU="Guillot, Loic"
  27. AU=Pocrnic Ivan
  28. AU="Rackova, Sylva"
  29. AU="Jordan Denizeau"
  30. AU="Alexandra J. Corbett"
  31. AU="Felderman, Howard E"
  32. AU="Chen, Fuxing"
  33. AU="Soekadar, Surjo R"
  34. AU="Pagotto, Sara"
  35. AU="Dominguez, Georgina Cutillas"
  36. AU=Barabutis Nektarios
  37. AU="Rumalla, Kavelin"
  38. AU=Meares Gordon P.
  39. AU="Gawron, Lori M"
  40. AU=Guettari Moez
  41. AU=Ma Xingcong
  42. AU="Greene, Kerrie" AU="Greene, Kerrie"
  43. AU="Adebayo, Abe"
  44. AU=Amoako Yaw Ampem
  45. AU="Khanna, Sakshum"

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  1. Artikel ; Online: Advances and Challenges in Diagnosis and Management of Heart Failure

    Ryan D. Sullivan / Inna P. Gladysheva

    Diagnostics, Vol 12, Iss 1103, p

    2022  Band 1103

    Abstract: The prevalence of heart failure (HF) with reduced (r) and preserved (p) ejection fraction (EF) continues to rise globally despite current advances in diagnostics and improvements to medical management [.] ...

    Abstract The prevalence of heart failure (HF) with reduced (r) and preserved (p) ejection fraction (EF) continues to rise globally despite current advances in diagnostics and improvements to medical management [.]
    Schlagwörter n/a ; Medicine (General) ; R5-920
    Sprache Englisch
    Erscheinungsdatum 2022-04-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: Sodium-Glucose Cotransporter-2 Inhibitors Improve Heart Failure with Reduced Ejection Fraction Outcomes by Reducing Edema and Congestion

    Michelle Hernandez / Ryan D. Sullivan / Mariana E. McCune / Guy L. Reed / Inna P. Gladysheva

    Diagnostics, Vol 12, Iss 989, p

    2022  Band 989

    Abstract: Pathological sodium-water retention or edema/congestion is a primary cause of heart failure (HF) decompensation, clinical symptoms, hospitalization, reduced quality of life, and premature mortality. Sodium-glucose cotransporter-2 inhibitors (SGLT-2i) ... ...

    Abstract Pathological sodium-water retention or edema/congestion is a primary cause of heart failure (HF) decompensation, clinical symptoms, hospitalization, reduced quality of life, and premature mortality. Sodium-glucose cotransporter-2 inhibitors (SGLT-2i) based therapies reduce hospitalization due to HF, improve functional status, quality, and duration of life in patients with HF with reduced ejection fraction (HFrEF) independently of their glycemic status. The pathophysiologic mechanisms and molecular pathways responsible for the benefits of SGLT-2i in HFrEF remain inconclusive, but SGLT-2i may help HFrEF by normalizing salt-water homeostasis to prevent clinical edema/congestion. In HFrEF, edema and congestion are related to compromised cardiac function. Edema and congestion are further aggravated by renal and pulmonary abnormalities. Treatment of HFrEF patients with SGLT-2i enhances natriuresis/diuresis, improves cardiac function, and reduces natriuretic peptide plasma levels. In this review, we summarize current clinical research studies related to outcomes of SGLT-2i treatment in HFrEF with a specific focus on their contribution to relieving or preventing edema and congestion, slowing HF progression, and decreasing the rate of rehospitalization and cardiovascular mortality.
    Schlagwörter HFrEF ; edema ; congestion ; dilated cardiomyopathy ; fluid management ; endothelial dysfunction ; Medicine (General) ; R5-920
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2022-04-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: A Low-Sodium Diet Boosts Ang (1–7) Production and NO-cGMP Bioavailability to Reduce Edema and Enhance Survival in Experimental Heart Failure

    Ranjana Tripathi / Ryan D. Sullivan / Tai-Hwang M. Fan / Radhika M. Mehta / Inna P. Gladysheva / Guy L. Reed

    International Journal of Molecular Sciences, Vol 22, Iss 4035, p

    2021  Band 4035

    Abstract: Sodium restriction is often recommended in heart failure (HF) to block symptomatic edema, despite limited evidence for benefit. However, a low-sodium diet (LSD) activates the classical renin-angiotensin-aldosterone system (RAAS), which may adversely ... ...

    Abstract Sodium restriction is often recommended in heart failure (HF) to block symptomatic edema, despite limited evidence for benefit. However, a low-sodium diet (LSD) activates the classical renin-angiotensin-aldosterone system (RAAS), which may adversely affect HF progression and mortality in patients with dilated cardiomyopathy (DCM). We performed a randomized, blinded pre-clinical trial to compare the effects of a normal (human-equivalent) sodium diet and a LSD on HF progression in a normotensive model of DCM in mice that has translational relevance to human HF. The LSD reduced HF progression by suppressing the development of pleural effusions ( p < 0.01), blocking pathological increases in systemic extracellular water ( p < 0.001) and prolonging median survival (15%, p < 0.01). The LSD activated the classical RAAS by increasing plasma renin activity, angiotensin II and aldosterone levels. However, the LSD also significantly up-elevated the counter-regulatory RAAS by boosting plasma angiotensin converting enzyme 2 (ACE2) and angiotensin (1–7) levels, promoting nitric oxide bioavailability and stimulating 3′-5′-cyclic guanosine monophosphate (cGMP) production. Plasma HF biomarkers associated with poor outcomes, such as B-type natriuretic peptide and neprilysin were decreased by a LSD. Cardiac systolic function, blood pressure and renal function were not affected. Although a LSD activates the classical RAAS system, we conclude that the LSD delayed HF progression and mortality in experimental DCM, in part through protective stimulation of the counter-regulatory RAAS to increase plasma ACE2 and angiotensin (1–7) levels, nitric oxide bioavailability and cGMP production.
    Schlagwörter dietary sodium restriction ; dilated cardiomyopathy ; edema ; nitric oxide ; angiotensin (1–7) ; ACE-2 ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2021-04-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  4. Artikel ; Online: Renin Activity in Heart Failure with Reduced Systolic Function—New Insights

    Ryan D. Sullivan / Radhika M. Mehta / Ranjana Tripathi / Guy L. Reed / Inna P. Gladysheva

    International Journal of Molecular Sciences, Vol 20, Iss 13, p

    2019  Band 3182

    Abstract: Regardless of the cause, symptomatic heart failure (HF) with reduced ejection fraction (rEF) is characterized by pathological activation of the renin−angiotensin−aldosterone system (RAAS) with sodium retention and extracellular fluid expansion (edema). ... ...

    Abstract Regardless of the cause, symptomatic heart failure (HF) with reduced ejection fraction (rEF) is characterized by pathological activation of the renin−angiotensin−aldosterone system (RAAS) with sodium retention and extracellular fluid expansion (edema). Here, we review the role of active renin, a crucial, upstream enzymatic regulator of the RAAS, as a prognostic and diagnostic plasma biomarker of heart failure with reduced ejection fraction (HFrEF) progression; we also discuss its potential as a pharmacological bio-target in HF therapy. Clinical and experimental studies indicate that plasma renin activity is elevated with symptomatic HFrEF with edema in patients, as well as in companion animals and experimental models of HF. Plasma renin activity levels are also reported to be elevated in patients and animals with rEF before the development of symptomatic HF. Modulation of renin activity in experimental HF significantly reduces edema formation and the progression of systolic dysfunction and improves survival. Thus, specific assessment and targeting of elevated renin activity may enhance diagnostic and therapeutic precision to improve outcomes in appropriate patients with HFrEF.
    Schlagwörter heart failure ; plasma renin activity ; renin–angiotensin–aldosterone system ; renin ; prorenin ; (pro)renin receptor ; reduced systolic function ; dilated cardiomyopathy ; direct renin inhibitor ; aldosterone ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2019-06-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  5. Artikel ; Online: Normalizing Plasma Renin Activity in Experimental Dilated Cardiomyopathy

    Ryan D. Sullivan / Radhika M. Mehta / Ranjana Tripathi / Inna P. Gladysheva / Guy L. Reed

    International Journal of Molecular Sciences, Vol 20, Iss 16, p

    Effects on Edema, Cachexia, and Survival

    2019  Band 3886

    Abstract: Heart failure (HF) patients frequently have elevated plasma renin activity. We examined the significance of elevated plasma renin activity in a translationally-relevant model of dilated cardiomyopathy (DCM), which replicates the progressive stages (A−D) ... ...

    Abstract Heart failure (HF) patients frequently have elevated plasma renin activity. We examined the significance of elevated plasma renin activity in a translationally-relevant model of dilated cardiomyopathy (DCM), which replicates the progressive stages (A−D) of human HF. Female mice with DCM and elevated plasma renin activity concentrations were treated with a direct renin inhibitor (aliskiren) in a randomized, blinded fashion beginning at Stage B HF. By comparison to controls, aliskiren treatment normalized pathologically elevated plasma renin activity ( p < 0.001) and neprilysin levels ( p < 0.001), but did not significantly alter pathological changes in plasma aldosterone, angiotensin II, atrial natriuretic peptide, or corin levels. Aliskiren improved cardiac systolic function (ejection fraction, p < 0.05; cardiac output, p < 0.01) and significantly reduced the longitudinal development of edema (extracellular water, p < 0.0001), retarding the transition from Stage B to Stage C HF. The normalization of elevated plasma renin activity reduced the loss of body fat and lean mass (cachexia/sarcopenia), p < 0.001) and prolonged survival ( p < 0.05). In summary, the normalization of plasma renin activity retards the progression of experimental HF by improving cardiac systolic function, reducing the development of systemic edema, cachexia/sarcopenia, and mortality. These data suggest that targeting pathologically elevated plasma renin activity may be beneficial in appropriately selected HF patients.
    Schlagwörter plasma renin activity ; heart failure ; aliskiren ; dilated cardiomyopathy ; neprilysin ; edema ; cachexia/sarcopenia ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2019-08-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  6. Artikel ; Online: In Experimental Dilated Cardiomyopathy Heart Failure and Survival Are Adversely Affected by a Lack of Sexual Interactions

    Ranjana Tripathi / Ryan D. Sullivan / Tai-Hwang M. Fan / Radhika M. Mehta / Inna P. Gladysheva / Guy L. Reed

    International Journal of Molecular Sciences, Vol 21, Iss 5450, p

    2020  Band 5450

    Abstract: Nearly one in three people in the U.S. will develop heart failure (HF), characterized by fluid retention (edema) in the lungs and elsewhere. This leads to difficult breathing, deterioration of physical capacity, restriction of normal activities and death. ...

    Abstract Nearly one in three people in the U.S. will develop heart failure (HF), characterized by fluid retention (edema) in the lungs and elsewhere. This leads to difficult breathing, deterioration of physical capacity, restriction of normal activities and death. There is little data about the safety and effects of sexual interactions in patients with HF. We tested whether a lack of sexual interactions affected pathophysiological outcomes in a pre-clinical mouse model of dilated cardiomyopathy that recapitulates the progressive stages of human HF. Male mice were randomly given access to, or deprived from, sexual interactions with female mice, which were confirmed by videography and generation of offspring. Cohousing with access to sexual interactions markedly prolonged survival, while cohousing without access to sexual activity did not. Sexual interactions improved systolic function, reduced HF-associated edema, altered transcription of heart contractile protein genes and decreased plasma testosterone levels. To determine whether testosterone levels contributed to survival, testosterone levels were experimentally reduced. Reduction of testosterone levels significantly prolonged survival. Taken together, in mice with dilated cardiomyopathy, sexual activity altered cardiac contractile gene transcription, improved systolic function, reduced edema and prolonged survival which may be in part due to lower testosterone levels.
    Schlagwörter heart failure ; dilated cardiomyopathy ; edema ; pleural effusion ; contractile function ; testosterone ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Sprache Englisch
    Erscheinungsdatum 2020-07-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  7. Artikel ; Online: Corin Overexpression Reduces Myocardial Infarct Size and Modulates Cardiomyocyte Apoptotic Cell Death

    Ryan D. Sullivan / Aiilyan K. Houng / Inna P. Gladysheva / Tai-Hwang M. Fan / Ranjana Tripathi / Guy L. Reed / Dong Wang

    International Journal of Molecular Sciences, Vol 21, Iss 3456, p

    2020  Band 3456

    Abstract: Altered expression of corin, a cardiac transmembrane serine protease, has been linked to dilated and ischemic cardiomyopathy. However, the potential role of corin in myocardial infarction (MI) is lacking. This study examined the outcomes of MI in wild- ... ...

    Abstract Altered expression of corin, a cardiac transmembrane serine protease, has been linked to dilated and ischemic cardiomyopathy. However, the potential role of corin in myocardial infarction (MI) is lacking. This study examined the outcomes of MI in wild-type vs. cardiac-specific overexpressed corin transgenic (Corin-Tg) mice during pre-MI, early phase (3, 24, 72 h), and late phase (1, 4 weeks) post-MI. Corin overexpression significantly reduced cardiac cell apoptosis ( p < 0.001), infarct size ( p < 0.001), and inhibited cleavage of procaspases 3, 9, and 8 ( p < 0.05 to p < 0.01), as well as altered the expression of Bcl2 family proteins, Bcl-xl, Bcl2 and Bak ( p < 0.05 to p < 0.001) at 24 h post-MI. Overexpressed cardiac corin also significantly modulated heart function (ejection fraction, p < 0.0001), lung congestion (lung weight to body weight ratio, p < 0.0001), and systemic extracellular water (edema, p < 0.05) during late phase post-MI. Overall, cardiac corin overexpression significantly reduced apoptosis, infarct size, and modulated cardiac expression of key members of the apoptotic pathway in early phase post-MI; and led to significant improvement in heart function and reduced congestion in late phase post-MI. These findings suggest that corin may be a useful target to protect the heart from ischemic injury and subsequent post-infarction remodeling.
    Schlagwörter myocardial infarction ; corin ; apoptosis ; Bcl-2 family protein ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2020-05-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  8. Artikel ; Online: Enhanced heart failure, mortality and renin activation in female mice with experimental dilated cardiomyopathy.

    Ranjana Tripathi / Ryan Sullivan / Tai-Hwang M Fan / Dong Wang / Yao Sun / Guy L Reed / Inna P Gladysheva

    PLoS ONE, Vol 12, Iss 12, p e

    2017  Band 0189315

    Abstract: Dilated cardiomyopathy (DCM) is the major cause of heart failure affecting both women and men. Limited clinical studies show conflicting data in sex-related differences in the progression of dilated cardiomyopathy and heart failure (HF) outcomes. We ... ...

    Abstract Dilated cardiomyopathy (DCM) is the major cause of heart failure affecting both women and men. Limited clinical studies show conflicting data in sex-related differences in the progression of dilated cardiomyopathy and heart failure (HF) outcomes. We examined the comparative sex-related progression of cardiomyopathy and the development of HF (at 4, 7, 13 weeks of age) in a well-established, transgenic mouse model of DCM that recapitulates the progressive stages of human HF. By 13 weeks of age, female mice with DCM had more severe left ventricular systolic dysfunction, left ventricular dilation and wall thinning (P<0.001 for all) than age-matched male mice with DCM. Female mice also had greater lung edema (P<0.001), cardiac fibrosis (P<0.01) and pleural effusions, which were not rescued by ovariectomy. By comparison to DCM male mice at 13 weeks, these pathological changes in female mice with DCM, were associated with significant increases in plasma active renin (P<0.01), angiotensin II (P<0.01) and aldosterone levels (P<0.001). In comparison to DCM male mice, DCM female mice also showed differential expression of the natriuretic peptide system with lower corin and higher ANP, BNP and cGMP levels at 13 weeks of age. We conclude, that female mice with experimental DCM have an accelerated progression of cardiomyopathy and HF, which was not corrected by early ovariectomy. These alterations are associated with early renin activation with increased angiotensin II and aldosterone levels, and altered expression of the natriuretic peptide system.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 630
    Sprache Englisch
    Erscheinungsdatum 2017-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  9. Artikel ; Online: Cardiac-Specific Overexpression of Catalytically Inactive Corin Reduces Edema, Contractile Dysfunction, and Death in Mice with Dilated Cardiomyopathy

    Ranjana Tripathi / Ryan D. Sullivan / Tai-Hwang M. Fan / Aiilyan K. Houng / Radhika M. Mehta / Guy L. Reed / Inna P. Gladysheva

    International Journal of Molecular Sciences, Vol 21, Iss 1, p

    2019  Band 203

    Abstract: Humans with dilated cardiomyopathy (DCM) and heart failure (HF) develop low levels of corin, a multi-domain, cardiac-selective serine protease involved in natriuretic peptide cleavage and sodium and water regulation. However, experimental restoration of ... ...

    Abstract Humans with dilated cardiomyopathy (DCM) and heart failure (HF) develop low levels of corin, a multi-domain, cardiac-selective serine protease involved in natriuretic peptide cleavage and sodium and water regulation. However, experimental restoration of corin levels markedly attenuates HF progression. To determine whether the beneficial effects of corin in HF require catalytic activity, we engineered cardiac overexpression of an enzymatically inactive corin transgene (corin-Tg(i)). On a wild-type (WT) background, corin-Tg(i) had no evident phenotypic effects. However, in a well-established genetic model of DCM, corin-Tg(i)/DCM mice had increased survival ( p < 0.01 to 0.001) vs. littermate corin-WT/DCM controls. Pleural effusion ( p < 0.01), lung edema ( p < 0.05), systemic extracellular free water ( p < 0.01), and heart weight were decreased ( p < 0.01) in corin-Tg(i)/DCM vs. corin-WT/DCM mice. Cardiac ejection fraction and fractional shortening improved ( p < 0.01), while ventricular dilation decreased ( p < 0.0001) in corin-Tg(i)/DCM mice. Plasma atrial natriuretic peptide, cyclic guanosine monophosphate, and neprilysin were significantly decreased. Cardiac phosphorylated glycogen synthase kinase-3β (pSer9-GSK3β) levels were increased in corin(i)-Tg/DCM mice ( p < 0.01). In summary, catalytically inactive corin-Tg(i) decreased fluid retention, improved contractile function, decreased HF biomarkers, and diminished cardiac GSK3β activity. Thus, the protective effects of cardiac corin on HF progression and survival in experimental DCM do not require the serine protease activity of the molecule.
    Schlagwörter corin ; dilated cardiomyopathy ; heart failure ; edema ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Sprache Englisch
    Erscheinungsdatum 2019-12-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  10. Artikel ; Online: Increases in plasma corin levels following experimental myocardial infarction reflect the severity of ischemic injury.

    Dong Wang / Inna P Gladysheva / Ryan D Sullivan / Tai-Hwang M Fan / Radhika M Mehta / Ranjana Tripathi / Yao Sun / Guy L Reed

    PLoS ONE, Vol 13, Iss 9, p e

    2018  Band 0202571

    Abstract: Following acute myocardial infarction, clinical studies show alterations in the blood levels of corin, a cardiac-selective activator of the natriuretic peptides pro-atrial natriuretic peptide (pro-ANP) and pro-B-type natriuretic peptide (pro-BNP). ... ...

    Abstract Following acute myocardial infarction, clinical studies show alterations in the blood levels of corin, a cardiac-selective activator of the natriuretic peptides pro-atrial natriuretic peptide (pro-ANP) and pro-B-type natriuretic peptide (pro-BNP). However, the temporal changes in circulating and cardiac corin levels and their relationships to the severity of myocardial infarction have not been studied. The main objective of this study was to examine the relationship between cardiac and circulating corin levels and their association with cardiac systolic function and infarct size during the early phase of acute myocardial infarction (<72 h) in a translationally relevant induced coronary ligation mouse model. This acute phase timeline was chosen to correlate with the clinical practice within which blood samples are collected from myocardial infarction patients. Heart and plasma samples were examined at 3, 24, and 72 hours post acute myocardial infarction. Plasma corin levels were examined by enzyme-linked immunosorbent assay, transcripts of cardiac corin, pro-ANP and pro-BNP by quantitative real-time polymerase chain reaction, cardiac corin expression by immunohistology, infarct size by histology and heart function by echocardiography. Plasma corin levels were significantly increased at 3 (P<0.05), 24 (P<0.001), and 72 hours (P<0.01) post-acute myocardial infarction. In contrast, cardiac corin transcript levels dropped by 5% (P>0.05), 69% (P<0.001) and 65% (P<0.001) and immunoreactive cardiac corin protein levels dropped by 30% (P<0.05), 76% (P<0.001) and 75% (P<0.001), while cardiac pro-ANP and pro-BNP transcript levels showed an opposite pattern. Plasma corin levels were negatively correlated with immunoreactive cardiac corin (P<0.01), ejection fraction (P<0.05) and fractional shortening (P<0.05), but positively correlated with infarct size (P<0.01). In conclusion, acute myocardial infarction induces rapid increases in plasma corin and decreases in cardiac corin levels. ...
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2018-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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