Elevated plasma S100A1 level is a risk factor for ST-segment elevation myocardial infarction and associated with post-infarction cardiac function

Fan, Linlin; Liu, Baoxin; Guo, Rong; Luo, Jiachen; Li, Hongqiang; Li, Zhiqiang; Xu, Weigang

doi:10.7150/ijms.35037

Cited by 10 publications

(11 citation statements)

References 52 publications

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“…S100A1 seems to be an essential factor concerning cardiological diseases since it is involved in the contractile performance of cardiomyocytes [36,37]. Fan et al demonstrated that patients showing ST-segment elevation myocardial infarction (STEMI) in the electrocardiogram (ECG) also had increased levels of S100A1 and that this S100 family member could complement current biomarkers [67]. It was also shown that S100A1 concentrations rise during early-stage acute myocardial ischemia, followed by a quick decrease, and thereby S100A1 could represent an early biomarker [68].…”

Section: Clinical Relevance Of S100 Proteinsmentioning

confidence: 99%

Friend or Foe: S100 Proteins in Cancer

Allgöwer

Kretz

Karstedt

et al. 2020

Cancers

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S100 proteins are widely expressed small molecular EF-hand calcium-binding proteins of vertebrates, which are involved in numerous cellular processes, such as Ca2+ homeostasis, proliferation, apoptosis, differentiation, and inflammation. Although the complex network of S100 signalling is by far not fully deciphered, several S100 family members could be linked to a variety of diseases, such as inflammatory disorders, neurological diseases, and also cancer. The research of the past decades revealed that S100 proteins play a crucial role in the development and progression of many cancer types, such as breast cancer, lung cancer, and melanoma. Hence, S100 family members have also been shown to be promising diagnostic markers and possible novel targets for therapy. However, the current knowledge of S100 proteins is limited and more attention to this unique group of proteins is needed. Therefore, this review article summarises S100 proteins and their relation in different cancer types, while also providing an overview of novel therapeutic strategies for targeting S100 proteins for cancer treatment.

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Section: Clinical Relevance Of S100 Proteinsmentioning

confidence: 99%

Friend or Foe: S100 Proteins in Cancer

Allgöwer

Kretz

Karstedt

et al. 2020

Cancers

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“…Among the S100 family, S100A1 has the highest concentration in the myocardium, and its protein concentration level determines the likelihood of heart failure and contractile function following myocardial infarction (Rohde et al, 2014). Studies have shown that an elevated plasma S100A1 level is a significant predictor of STsegment elevation myocardial infarction, while there is reduced S100A1 expression in failing and hypertrophic heart tissues (Fan et al, 2019). The restoration of S100A1 expression to normal levels in failing cardiomyocytes using gene therapy can improve myocardial contractile function (Bennett et al, 2014;Brinks et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Reynoutrin Improves Ischemic Heart Failure in Rats Via Targeting S100A1

Yang

Tang

et al. 2021

Front. Pharmacol.

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This study investigated the effects of reynoutrin on the improvement of ischemic heart failure (IHF) and its possible mechanism in rats. The rat heart failure model was established by permanently ligating the left anterior descending coronary artery (LAD) and administering different doses of reynoutrin. Cardiac function, inflammatory factors releasing, oxidative stress, cardiomyocytes apoptosis, and myocardial fibrosis were evaluated. Western blotting was used to determine protein expression levels of S100 calcium-binding protein A1 (S100A1), matrix metallopeptidase 2(MMP2), MMP9, phosphorylated (p-) p65, and transforming growth factor -β1 (TGF-β1) in myocardial tissue of the left ventricle. Results showed that reynoutrin significantly improved cardiac function, suppressed the release of inflammatory factors, reduced oxidative stress, inhibited cardiomyocytes apoptosis, and attenuated myocardial fibrosis in rats with IHF. In rat myocardial tissue, permanent LAD-ligation resulted in a significant down-regulation in S100A1 expression, whereas reynoutrin significantly up-regulated S100A1 protein expression while down-regulating MMP2, MMP9, p-p65, and TGF-β1 expressions. However, when S100A1 was knocked down in myocardial tissue, the above-mentioned positive effects of reynoutrin were significantly reversed. Reynoutrin is a potential natural drug for the treatment of IHF, and its mechanism of action involves the up-regulation of S100A1 expression, thereby inhibiting expressions of MMPs and the transcriptional activity of nuclear factor kappa-B.

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“…S100A1, a predominant member of the S100 protein family, is a crucial regulator of cardiac contractility. Due to its ability to enhance sarcoplasmic reticulum Ca 2+ fluxes and increase SERCA2a enzyme activity, it can lead to the significant limitation of myocardial necrosis and development of HF [120]. A recent study conducted by Jungi and colleagues reported that S100A1 gene overexpression through the AAV9 vector can have cardioprotective effects in male Lewis rats after IRI.…”

Section: Gene Therapy To Reduce Apoptosismentioning

confidence: 99%

Recent Advances in Gene Therapy for Cardiac Tissue Regeneration

Kim

Zharkinbekov

Sarsenova

et al. 2021

IJMS

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Cardiovascular diseases (CVDs) are responsible for enormous socio-economic impact and the highest mortality globally. The standard of care for CVDs, which includes medications and surgical interventions, in most cases, can delay but not prevent the progression of disease. Gene therapy has been considered as a potential therapy to improve the outcomes of CVDs as it targets the molecular mechanisms implicated in heart failure. Cardiac reprogramming, therapeutic angiogenesis using growth factors, antioxidant, and anti-apoptotic therapies are the modalities of cardiac gene therapy that have led to promising results in preclinical studies. Despite the benefits observed in animal studies, the attempts to translate them to humans have been inconsistent so far. Low concentration of the gene product at the target site, incomplete understanding of the molecular pathways of the disease, selected gene delivery method, difference between animal models and humans among others are probable causes of the inconsistent results in clinics. In this review, we discuss the most recent applications of the aforementioned gene therapy strategies to improve cardiac tissue regeneration in preclinical and clinical studies as well as the challenges associated with them. In addition, we consider ongoing gene therapy clinical trials focused on cardiac regeneration in CVDs.

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Elevated plasma S100A1 level is a risk factor for ST-segment elevation myocardial infarction and associated with post-infarction cardiac function

Cited by 10 publications

References 52 publications

Friend or Foe: S100 Proteins in Cancer

Friend or Foe: S100 Proteins in Cancer

Reynoutrin Improves Ischemic Heart Failure in Rats Via Targeting S100A1

Recent Advances in Gene Therapy for Cardiac Tissue Regeneration

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