Cerebral derailment after myocardial infarct: mechanisms and effects of the signaling from the ischemic heart to brain

Castiglioni, Laura; Rzemieniec, Joanna; Muluhie, Majeda; Camera, Marina; Sironi, Luigi

doi:10.1007/s00109-021-02154-3

Cited by 9 publications

(2 citation statements)

References 160 publications

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“…Therefore, EVs are considered important mediators of heart–brain interactions. Furthermore, miR-1, miR-133, mir-208a, and miR-499, which are considered to be cardiac-specific, were also clearly altered in the plasma of MI patients ( 98 ). Previous studies indicate that exosomes transport cardiac-derived miR-1 into hippocampal neurons following MI and disrupt the microtubule structure of mouse hippocampal neurons by suppressing the expression of TPPP/p25 protein ( 99 ).…”

Section: Potential Mechanisms Of Cardiogenic Dementiamentioning

confidence: 99%

Heart–brain interaction in cardiogenic dementia: pathophysiology and therapeutic potential

Liu,

Xiao,

Liang

et al. 2024

Front. Cardiovasc. Med.

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Diagnosis and treatment of patients with cardiovascular and neurologic diseases primarily focus on the heart and brain, respectively. An increasing number of preclinical and clinical studies have confirmed a causal relationship between heart and brain diseases. Cardiogenic dementia is a cognitive impairment caused by heart dysfunction and has received increasing research attention. The prevention and treatment of cardiogenic dementia are essential to improve the quality of life, particularly in the elderly and aging population. This study describes the changes in cognitive function associated with coronary artery disease, myocardial infarction, heart failure, atrial fibrillation and heart valve disease. An updated understanding of the two known pathogenic mechanisms of cardiogenic dementia is presented and discussed. One is a cascade of events caused by cerebral hypoperfusion due to long-term reduction of cardiac output after heart disease, and the other is cognitive impairment regardless of the changes in cerebral blood flow after cardiac injury. Furthermore, potential medications for the prevention and treatment of cardiogenic dementia are reviewed, with particular attention to multicomponent herbal medicines.

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Section: Potential Mechanisms Of Cardiogenic Dementiamentioning

confidence: 99%

Heart–brain interaction in cardiogenic dementia: pathophysiology and therapeutic potential

Liu,

Xiao,

Liang

et al. 2024

Front. Cardiovasc. Med.

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“…The costs of CVDs treatment impose a substantial economic burden on society. Myocardial infarction (MI) is one of the significant ischemic heart diseases ( Gelosa et al, 2022 ). When the coronary artery is blocked or stenosed, the blood supply to the heart is reduced or stopped, eventually causing MI ( Vogel et al, 2019 ; Cohen et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

Network pharmacology-based and experimental identification of the effects of Renshen Yangrong decoction on myocardial infarction

Zhao

Xu²,

Yang³

2022

Front. Pharmacol.

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Objective: Myocardial infarction (MI) is one of the leading causes of death worldwide. Currently, the drugs used to treat MI have various side effects. Emerging evidence supports the protective effects of Renshen Yangrong Decoction (RSYRD) in cardiovascular diseases (CVDs) treatments, with few side effect reports. However, the role of RSYRD in MI remains unclear. In this study, network pharmacological analysis was combined with experiments in vivo and in vitro to validate the effects of RSYRD in the treatment during the early stage of MI.Methods: Firstly, network pharmacology analysis was performed to search for the potential targets and signaling pathways of RSYRD in the early stage of MI. Then, the protein-protein interaction (PPI) network was constructed to identify the core genes of RSYRD that may play a key role in MI. At last, the treatment effectiveness of RSYRD on MI was verified via experiments in vitro and in vivo.Results: RSYRD contained fifty-six bioactive components. Eighty-eight intersections between RSYRD and MI targets and thirteen core genes were screened. KEGG and GO functional enrichment analyses predicted that RSYRD might play a therapeutic role in MI through oxidative stress, apoptosis, and immune-inflammatory signaling pathways. In vivo and in vitro experiment results revealed that significant apoptosis occurred in myocardial tissue in the early stage of MI. Moreover, the levels of reactive oxide species (ROS), TNF-α, and IL-6 increased markedly. After RSYRD administration, they significantly decreased. At the mechanistic level, RSYRD could reduce ROS production to alleviate cell apoptosis.Conclusion: RSYRD could reduce neonatal mouse cardiomyocytes (NMCMs) apoptosis by lowering ROS production induced by hypoxia and improve the cardiac function of mice 3 days post-MI. RSYRD could also reduce the levels of TNF-α and IL-6 in the serum of mice.

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Spinal cord astrocytes regulate myocardial ischemia–reperfusion injury

Liu

Luo

et al. 2022

Basic Res Cardiol

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Cerebral derailment after myocardial infarct: mechanisms and effects of the signaling from the ischemic heart to brain

Cited by 9 publications

References 160 publications

Heart–brain interaction in cardiogenic dementia: pathophysiology and therapeutic potential

Heart–brain interaction in cardiogenic dementia: pathophysiology and therapeutic potential

Network pharmacology-based and experimental identification of the effects of Renshen Yangrong decoction on myocardial infarction

Spinal cord astrocytes regulate myocardial ischemia–reperfusion injury

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