Role of inflammation in the pathogenesis of cardiorenal syndrome in a rat myocardial infarction model

Cho, Eun Jung; Kim, Mina; Ko, Yoon Sook; Lee, Hee Young; Song, Myeongjin; Kim, Myung Gyu; Kim, Hyoung Kyu; Cho, Won Yong; Jo, Sang Kyung

doi:10.1093/ndt/gft376

Cited by 49 publications

(53 citation statements)

References 18 publications

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“…The inflammatory cytokines, IL-6, and tumor necrosis factor-α (TNF-α) mRNA expression, as well as microvascular endothelial permeability and tubular cell apoptosis, significantly enhanced in the kidneys of MI rats. These findings support the involvement of the immune activation/inflammation in the pathophysiology of CRS besides the hemodynamic alteration, pathological compensatory neurohormonal activation and oxidative stress (76). …”

Section: The Contribution Of the Immune System To Heart Failuresupporting

confidence: 81%

“…Moreover, macrophage infiltration and inflammatory cytokine expression possibly mediated by the NF-κB pathway, and microvascular endothelial damage increased significantly in kidneys at 3 days post-induction of MI, suggesting the important contribution of inflammation in the pathogenesis of type I CRS. These changes ultimately led to renal interstitial fibrosis along with chronically decreased heart function (type II CRS) (76). Although the direct effects of cytokines on ion transports in the kidney were no studied yet, the observation that heart failure is associated with enhanced renal TNF-α and IL-6 expression along tubular cell apoptosis supports such a role.…”

Section: The Contribution Of the Immune System To Heart Failurementioning

confidence: 99%

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Involvement of Cytokines in the Pathogenesis of Salt and Water Imbalance in Congestive Heart Failure

et al. 2017

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Congestive heart failure (CHF) has become a major medical problem in the western world with high morbidity and mortality rates. CHF adversely affects several systems, mainly the kidneys and the lungs. While the involvement of the renin–angiotensin–aldosterone system and the sympathetic nervous system in the progression of cardiovascular, pulmonary, and renal dysfunction in experimental and clinical CHF is well established, the importance of pro-inflammatory mediators in the pathogenesis of this clinical setting is still evolving. In this context, CHF is associated with overexpression of pro-inflammatory cytokines, such as tumor necrosis factor-α, interleukin (IL)-1, and IL-6, which are activated in response to environmental injury. This family of cytokines has been implicated in the deterioration of CHF, where it plays an important role in initiating and integrating homeostatic responses both at the myocardium and circulatory levels. We and others showed that angiotensin II decreased the ability of the lungs to clear edema and enhanced the fibrosis process via phosphorylation of the mitogen-activated protein kinases p38 and p42/44, which are generally involved in cellular responses to pro-inflammatory cytokines. Literature data also indicate the involvement of these effectors in modulating ion channel activity. It has been reported that in heart failure due to mitral stenosis; there were varying degrees of vascular and other associated parenchymal changes such as edema and fibrosis. In this review, we will discuss the effects of cytokines and other inflammatory mediators on the kidneys and the lungs in heart failure; especially their role in renal and alveolar ion channels activity and fluid balance.

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Section: The Contribution Of the Immune System To Heart Failuresupporting

confidence: 81%

Section: The Contribution Of the Immune System To Heart Failurementioning

confidence: 99%

Involvement of Cytokines in the Pathogenesis of Salt and Water Imbalance in Congestive Heart Failure

et al. 2017

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“…Inflammation is an important risk factor for end-organ damage [3][4][5][6] and has been implicated in hypertension [7,8]. A growing body of evidence suggests that inflammatory cytokines play important roles in the pathophysiology of renal disease [5,9].…”

Section: Introductionmentioning

confidence: 99%

“…A growing body of evidence suggests that inflammatory cytokines play important roles in the pathophysiology of renal disease [5,9]. Several groups have implicated the role of circulatory cytokines in ESRD [10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Angiotensin II-induced hypertensive renal inflammation is mediated through HMGB1-TLR4 signaling in rat tubulo-epithelial cells

Nair

Ebenezer

Saini

et al. 2015

Experimental Cell Research

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“…In addition, histological and functional changes in the kidney may involve macrophage infiltration and interstitial fibrosis in the cortex [18]. Permeability of the microvessel endothelium and tubule cell apoptosis were increased in the kidneys of rats in which myocardial infarction was induced [19]. Together, these findings suggest the existence of specific mechanisms that make CRS1 a unique pathophysiological entity.…”

Section: Discussionmentioning

confidence: 99%

Incidence, Mortality and Positive Predictive Value of Type 1 Cardiorenal Syndrome in Acute Coronary Syndrome

et al. 2016

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ObjectivesTo determine whether the risk of cardiovascular mortality associated with cardiorenal syndrome subtype 1 (CRS1) in patients who were hospitalized for acute coronary syndrome (ACS) was greater than the expected risk based on the sum of its components, to estimate the predictive value of CRS1, and to determine whether the severity of CRS1 worsens the prognosis.MethodsFollow-up study of 1912 incident cases of ACS for 1 year after discharge. Cox regression models were estimated with time to event (in-hospital death, and readmission or death during the first year after discharge) as the dependent variable.ResultsThe incidence of CRS1 was 9.2/1000 person-days of hospitalization (95% CI = 8.1–10.5), but these patients accounted for 56.6% (95% CI = 47.4–65.) of all mortality. The positive predictive value of CRS1 was 29.6% (95% CI = 23.9–36.0) for in-hospital death, and 51.4% (95% CI = 44.8–58.0) for readmission or death after discharge. The risk of in-hospital death from CRS1 (RR = 18.3; 95% CI = 6.3–53.2) was greater than the sum of risks associated with either acute heart failure (RR = 7.6; 95% CI = 1.8–31.8) or acute kidney injury (RR = 2.8; 95% CI = 0.9–8.8). The risk of events associated with CRS1 also increased with syndrome severity, reaching a RR of 10.6 (95% CI = 6.2–18.1) for in-hospital death at the highest severity level.ConclusionsThe effect of CRS1 on in-hospital mortality is greater than the sum of the effects associated with each of its components, and it increases with the severity of the syndrome. CRS1 accounted for more than half of all mortality, and its positive predictive value approached 30% in-hospital and 50% after discharge.

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Role of inflammation in the pathogenesis of cardiorenal syndrome in a rat myocardial infarction model

Abstract: This study identifies the possible important role of inflammatory response as a mediator of heart-kidney crosstalk in CRS.

Cited by 49 publications

References 18 publications

Involvement of Cytokines in the Pathogenesis of Salt and Water Imbalance in Congestive Heart Failure

Involvement of Cytokines in the Pathogenesis of Salt and Water Imbalance in Congestive Heart Failure

Angiotensin II-induced hypertensive renal inflammation is mediated through HMGB1-TLR4 signaling in rat tubulo-epithelial cells

Incidence, Mortality and Positive Predictive Value of Type 1 Cardiorenal Syndrome in Acute Coronary Syndrome

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