Autonomic regulation of imbalance‑induced myocardial fibrosis and its mechanism in rats with cirrhosis

Yu, Shanshan; Sun, Lei; Wang, Hua; Jiang, Jue; Zhou, Qi

doi:10.3892/etm.2021.10472

Cited by 2 publications

(4 citation statements)

References 45 publications

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“…This suggests that the positive contractile response β-adrenergic and negative contractile response to M2-receptor are attenuated in cirrhotic hearts compared with controls (Jaue et al, 1997). A recent study demonstrated that both β1 and M2 receptor protein expressions are decreased in the myocardial tissues from cirrhotic rats induced by carbon tetrachloride (Yu et al, 2021). The difference might be due to the nature of liver injury in the animal models.…”

Section: M2-muscarinic Receptormentioning

confidence: 98%

“…The role of the microbiota in mediating cardiac disease outcomes has also been evaluated with studies finding perturbations in microbial content and metabolites potentially able to mediate cardiac dysfunction and thus overall cardiovascular disease outcomes (Beale et al, 2021). Taken together, the intra-abdominal changes associated with portal hypertension including mesenteric ischemia, alterations in gut barrier function with increase in intestinal permeability, luminal bacterial overgrowth and ultimately translocation of bacteria and or bacteria derived products that result in endotoxemia, can potentially lead to an elevation of systemic pro-inflammatory cytokines including, but not limited, to tumor necrosis factor alpha (TNFα), interleukin 1β (IL-1β) and interleukin-6 (IL-6) (Liu et al, 2000;Yu et al, 2021), that can then mediate downstream cardiac dysfunction. Currently there is a paucity of both experimental and clinical data evaluating the role of the microbiota in cirrhosis associated cardiomyopathy.…”

Section: Introductionmentioning

confidence: 99%

“…In cirrhosis, inflammatory cytokines TNFα, IL-1β (Liu et al, 2000) and IL-6 (Yu et al, 2021) are increased in cardiac tissue in cirrhotic animal models. The cardiac inflammation mediates damage to the heart which include apoptosis and hypertrophy of the cardiomyocytes, and increased rigidity of the cardiac membrane (Ma et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

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Pathogenic Mechanisms Underlying Cirrhotic Cardiomyopathy

Liu

Nguyen

Yoon

et al. 2022

Front. Netw. Physiol.

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Cardiac dysfunction associated with cirrhosis in the absence of preexisting heart disease is a condition known as cirrhotic cardiomyopathy (CCM). Cardiac abnormalities consist of enlargement of cardiac chambers, attenuated systolic and diastolic contractile responses to stress stimuli, and repolarization changes. CCM may contribute to cardiovascular morbidity and mortality after liver transplantation and other major surgeries, and also to the pathogenesis of hepatorenal syndrome. The underlying mechanisms of CCM are poorly understood and as such medical therapy is an area of unmet medical need. The present review focuses on the pathogenic mechanisms responsible for development of CCM. The two major concurrent mechanistic pathways are the inflammatory phenotype due to portal hypertension, and protein/lipid synthetic/metabolic defects due to cirrhosis and liver insufficiency. The inflammatory phenotype arises from intestinal congestion due to portal hypertension, resulting in bacteria/endotoxin translocation into the systemic circulation. The cytokine storm associated with inflammation, particularly TNFα acting via NFκB depresses cardiac function. They also stimulate two evanescent gases, nitric oxide and carbon monoxide which produce cardiodepression by cGMP. Inflammation also stimulates the endocannabinoid CB-1 pathway. These systems inhibit the stimulatory beta-adrenergic contractile pathway. The liver insufficiency of cirrhosis is associated with defective synthesis or metabolism of several substances including proteins and lipids/lipoproteins. The protein defects including titin and collagen contribute to diastolic dysfunction. Other protein abnormalities such as a switch of myosin heavy chain isoforms result in systolic dysfunction. Lipid biochemical changes at the cardiac sarcolemmal plasma membrane result in increased cholesterol:phospholipid ratio and decreased membrane fluidity. Final common pathway changes involve abnormal cardiomyocyte intracellular ion kinetics, particularly calcium. In conclusion, cirrhotic cardiomyopathy is caused by two pathways of cellular and molecular dysfunction/damage due to hepatic insufficiency and portal hypertension.

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Section: M2-muscarinic Receptormentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

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Pathogenic Mechanisms Underlying Cirrhotic Cardiomyopathy

Liu

Nguyen

Yoon

et al. 2022

Front. Netw. Physiol.

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“…Furthermore, an autopsy study has shown ventricular hypertrophy, cardiac valve calcification, interstitial edema, fibrosis in myocytes, and coronary artery atherosclerosis in cirrhotic patients [ 65 ]. Cardiomyopathy as systolic and diastolic abnormalities, inotropic and chronotropic dysfunction, increased plasma levels of myocardial enzymes, myocyte swelling and hypertrophy, and gross abnormalities in cardiomyocytes in histological examinations have also been reported in animal models of cirrhosis and HE [ 66 , 67 , 68 , 69 ]. Reduced response to vasoconstrictors and accumulation of circulatory vasodilators, such as nitric oxide, carbon monoxide, and endocannabinoids explain the suppression of systemic vascular resistance in liver failure [ 70 , 71 , 72 , 73 ].…”

Section: Factors That May Indirectly Affect the Efficacy Of Glymphati...mentioning

confidence: 99%

The Glymphatic System May Play a Vital Role in the Pathogenesis of Hepatic Encephalopathy: A Narrative Review

Sepehrinezhad

Larsen

Ahmadabad

et al. 2023

Cells

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Hepatic encephalopathy (HE) is a neurological complication of liver disease resulting in cognitive, psychiatric, and motor symptoms. Although hyperammonemia is a key factor in the pathogenesis of HE, several other factors have recently been discovered. Among these, the impairment of a highly organized perivascular network known as the glymphatic pathway seems to be involved in the progression of some neurological complications due to the accumulation of misfolded proteins and waste substances in the brain interstitial fluids (ISF). The glymphatic system plays an important role in the clearance of brain metabolic derivatives and prevents aggregation of neurotoxic agents in the brain ISF. Impairment of it will result in aggravated accumulation of neurotoxic agents in the brain ISF. This could also be the case in patients with liver failure complicated by HE. Indeed, accumulation of some metabolic by-products and agents such as ammonia, glutamine, glutamate, and aromatic amino acids has been reported in the human brain ISF using microdialysis technique is attributed to worsening of HE and correlates with brain edema. Furthermore, it has been reported that the glymphatic system is impaired in the olfactory bulb, prefrontal cortex, and hippocampus in an experimental model of HE. In this review, we discuss different factors that may affect the function of the glymphatic pathways and how these changes may be involved in HE.

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Autonomic regulation of imbalance‑induced myocardial fibrosis and its mechanism in rats with cirrhosis

Cited by 2 publications

References 45 publications

Pathogenic Mechanisms Underlying Cirrhotic Cardiomyopathy

Pathogenic Mechanisms Underlying Cirrhotic Cardiomyopathy

The Glymphatic System May Play a Vital Role in the Pathogenesis of Hepatic Encephalopathy: A Narrative Review

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