Roles of Biomarkers in Myocardial Fibrosis

Ding, Yanfang; Wang, Yuan; Zhang, Wanqin; Jia, Qiujin; Wang, Xiaoling; Li, Yanyang; Lv, Shichao; Zhang, Junping

doi:10.14336/ad.2020.0604

Cited by 42 publications

(32 citation statements)

References 148 publications

(157 reference statements)

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“…Through the screening of sequencing results, we found that HKE restored the expression of fibrosis markers Acta1 ( Schwartz et al, 1986 ) and Fn1 ( Knowlton et al, 1992 ), which were verified by qRT-PCR ( Figures 5A,B ). In addition, 12 collagen-coding genes, which are also fibrosis markers ( Ding et al, 2020 ), underwent significant changes after HKE intervention ( Supplementary Figure S6 ). Together, these results provide important insights into the molecular mechanism by which HK alleviates myocardial fibrosis.…”

Section: Resultsmentioning

confidence: 99%

Honokiol Ameliorates Post-Myocardial Infarction Heart Failure Through Ucp3-Mediated Reactive Oxygen Species Inhibition

Liu

Tang

et al. 2022

Front. Pharmacol.

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Post-myocardial infarction heart failure (post-MI HF) is one of the leading global causes of death, and current prevention and treatment methods still cannot avoid the increasing incidence. Honokiol (HK) has previously been reported to improve myocardial ischemia/reperfusion injury and reverse myocardial hypertrophy by activating Sirt1 and Sirt3. We suspect that HK may also have a therapeutic effect on post-MI HF. In this study, we aimed to investigate the efficacy and mechanism of HK in the treatment of post-MI HF. We found that HK inhibited myocardial reactive oxygen species (ROS) production, reduced myocardial fibrosis, and improved cardiac function in mice after MI. HK also reduced the abnormality of mitochondrial membrane potential (MMP) and apoptosis of cardiomyocytes caused by peroxide in neonatal cardiomyocytes. RNAseq results revealed that HK restored the transcriptome changes to a certain extent and significantly enhanced the expression of mitochondrial inner membrane uncoupling protein isoform 3 (Ucp3), a protein that inhibits the production of mitochondrial ROS, protects cardiomyocytes, and relieves heart failure after myocardial infarction (MI). In cardiomyocytes with impaired Ucp3 expression, HK cannot protect against the damage caused by peroxide. More importantly, in Ucp3 knockout mice, HK did not change the increase in the ROS level and cardiac function damage after MI. Taken together, our results suggest that HK can increase the expression of the cardioprotective protein Ucp3 and maintain MMP, thereby inhibiting the production of ROS after MI and ameliorating heart failure.

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Section: Resultsmentioning

confidence: 99%

Honokiol Ameliorates Post-Myocardial Infarction Heart Failure Through Ucp3-Mediated Reactive Oxygen Species Inhibition

Liu

Tang

et al. 2022

Front. Pharmacol.

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“…Fibrosis is known as the first stage of diabetic cardiomyopathy [ 60 ]. Fibrosis biomarkers, including TGF-β1, TGF-β2, and CTGF as fibrosismarkers, and FSP1, POSTEN, and FN-1 as tissue remodeling markers have been systematically examined [ 61 , 62 ]. We found that the expressions of these genes were all increased in diabetic hearts.…”

Section: Discussionmentioning

confidence: 99%

A Novel ALDH2 Activator AD-9308 Improves Diastolic and Systolic Myocardial Functions in Streptozotocin-Induced Diabetic Mice

et al. 2021

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Diabetes mellitus has reached epidemic proportion worldwide. One of the diabetic complications is cardiomyopathy, characterized by early left ventricular (LV) diastolic dysfunction, followed by development of systolic dysfunction and ventricular dilation at a late stage. The pathogenesis is multifactorial, and there is no effective treatment yet. In recent years, 4-hydroxy-2-nonenal (4-HNE), a toxic aldehyde generated from lipid peroxidation, is implicated in the pathogenesis of cardiovascular diseases. Its high bioreactivity toward proteins results in cellular damage. Mitochondrial aldehyde dehydrogenase 2 (ALDH2) is the major enzyme that detoxifies 4-HNE. The development of small-molecule ALDH2 activator provides an opportunity for treating diabetic cardiomyopathy. This study found that AD-9308, a water-soluble andhighly selective ALDH2 activator, can improve LV diastolic and systolic functions, and wall remodeling in streptozotocin-induced diabetic mice. AD-9308 treatment dose-dependently lowered serum 4-HNE levels and 4-HNE protein adducts in cardiac tissue from diabetic mice, accompanied with ameliorated myocardial fibrosis, inflammation, and apoptosis. Improvements of mitochondrial functions, sarco/endoplasmic reticulumcalcium handling and autophagy regulation were also observed in diabetic mice with AD-9308 treatment. In conclusion, ADLH2 activation effectively ameliorated diabetic cardiomyopathy, which may be mediated through detoxification of 4-HNE. Our findings highlighted the therapeutic potential of ALDH2 activation for treating diabetic cardiomyopathy.

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“…Cardiovascular biomarkers play an essential role in the diagnosis, risk stratification, and treatment of patients with cardiac diseases such as heart failure, dilated cardiomyopathy, and hypertrophic cardiomyopathy [24]. In recent years, much attention has been paid to searching for markers that would allow the noninvasive assessment of the degree of myocardial fibrosis and its possible consequences [20].…”

Section: Markers Of Fibrosismentioning

confidence: 99%

“…Endomyocardial biopsy is the gold standard in the diagnosis of myocardial fibrosis, but it has limitations in terms of clinical application. Biomarkers seem to be safer in diagnosis, treatment monitoring, and prognosis [24]. 4.1.…”

Section: Markers Of Fibrosismentioning

confidence: 99%

Cardiac fibrosis and atrial fibrillation

Mickiewicz

Lisowska

Knapp

2022

Postępy Higieny I Medycyny Doświadczalnej

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Cardiac fibrosis is characterized by the imbalance of production and degradation of the extracellular matrix. The result of this process is an accumulation of scar tissue, which is associated with many pathological processes such as excessive mechanical stress on the heart, inflammation, ischemia, oxidative stress, or excessive neurohormonal activation. Fibrotic response results in damaged heart architecture and dysfunction of the heart. Cardiac fibrosis leads to increased stiffness of the left ventricle and arteries, promotes disorders of contraction and relaxation of the heart, disrupts electrophysiology of heart cells, and induces arrhythmias. Atrial fibrillation is one of the most common arrhythmias. It is associated with a deterioration in the quality of life and more frequent use of medical assistance. It is also an instantaneous risk factor for many diseases, including stroke. The underlying cause of this arrhythmia is electrical and structural remodeling induced by cardiac fibrosis. Therefore, much attention is paid to the search for biochemical markers that would allow non-invasive determination of the degree of this fibrosis. The promising markers include galectin-3, human epididymis protein 4 (HE4), serum soluble ST2, and adipose triglyceride lipase (ATGL). Studies have shown that plasma concentrations of these substances reflect the degree of myocardial fibrosis and are indirectly associated with AF. There are high hopes for the use of these markers in patients undergoing arrhythmia ablation. More research is needed to confirm that these markers can be used to estimate the chance of maintaining sinus rhythm in patients after ablation.

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Roles of Biomarkers in Myocardial Fibrosis

Cited by 42 publications

References 148 publications

Honokiol Ameliorates Post-Myocardial Infarction Heart Failure Through Ucp3-Mediated Reactive Oxygen Species Inhibition

Honokiol Ameliorates Post-Myocardial Infarction Heart Failure Through Ucp3-Mediated Reactive Oxygen Species Inhibition

A Novel ALDH2 Activator AD-9308 Improves Diastolic and Systolic Myocardial Functions in Streptozotocin-Induced Diabetic Mice

Cardiac fibrosis and atrial fibrillation

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