Microarray analysis to evaluate different animal models for human heart failure

Ruíz, Patricia; Witt, Henning

doi:10.1016/j.yjmcc.2005.09.010

Cited by 10 publications

(11 citation statements)

References 14 publications

(14 reference statements)

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“…Human ischemic HF and canine HF share a similar overrepresentation of transcriptional pathways in the upregulated genes. However, in this study, no induction of prominent HF markers, such as atrial natriuretic peptides (ANPs), was detected 13 . After coronary ligation in the rat heart, LaFramboise and colleagues 14 demonstrated that transcripts for signal transduction and inflammation gene expression dominated in the infarct zone during late‐term recovery.…”

Section: Is Heart Failure Becoming a Molecular Disease?mentioning

confidence: 53%

Molecular mechanisms in evolutionary cardiology failure

Swynghedauw

Delcayre

Samuel

et al. 2010

Annals of the New York Academy of Sciences

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Integration of the relevant evolutionary paradigm in cardiology has not yet been fully achieved: In the past, heart failure (HF) was mainly ascribed to infections, and the origins of cardiac hypertrophy (CH) were regarded as mechanical. Recent changes in lifestyle have both reduced the incidence of infections and increased lifespan, and HF is now seen as a complex disease--one that is still caused by mechanical disorder, but also associated with ischemia and senescence. The long-held view that CH serves to restore myocardial economy back to normal is still valid. The adaptive process is characterized by a quantitative and a qualitative fetal gene reprogramming, which is now being confirmed by recent advances in microRNA research. It underscores the fact CH is the physiologic reaction of the heart to a pathologic stimulus. The goal for therapy is economic, not inotropic. Another major issue is myocardial fibrosis, a major determinant of diastolic function and arrhythmias. Recent changes in lifestyle have crucially modified the context in which HF occurs.

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Section: Is Heart Failure Becoming a Molecular Disease?mentioning

confidence: 53%

Molecular mechanisms in evolutionary cardiology failure

Swynghedauw

Delcayre

Samuel

et al. 2010

Annals of the New York Academy of Sciences

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“…Computer-assisted image analysis can raise the reproducibility of Ki-67 assessment [22], but it has a limited capacity of excluding normal stromal/inflammatory cells [23]. Also, tissue microarray technology has been introduced; its reliability and reproducibility were proven in studies [24]. A standardization of Ki-67 pathological assessment has not yet been accomplished [25].…”

Section: Discussionmentioning

confidence: 99%

Can Ki-67 Play a Role in Prediction of Breast Cancer Patients' Response to Neoadjuvant Chemotherapy?

Juhasz‐Böss¹,

Mavrova²,

Simona³

et al. 2014

BioMed Research International

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Background. Currently the choice of breast cancer therapy is based on prognostic factors. The proliferation marker Ki-67 is used increasingly to determine the method of therapy. The current study analyses the predictive value of Ki-67 in foreseeing breast cancer patients' responses to neoadjuvant chemotherapy. Methods. This study includes patients with invasive breast cancer treated between 2008 and 2013. The clinical response was assessed by correlating Ki-67 to histological examination, mammography, and ultrasonography findings. Results. The average Ki-67 value in our patients collectively (n = 77) is 34.9 ± 24.6%. The average Ki-67 value is the highest with 37.4 ± 24.0% in patients with a pCR. The Ki-67 values do not differ significantly among the 3 groups: pCR versus partial pathological response versus stable disease/progress (P = 0.896). However, Ki-67 values of patients with luminal, Her2 enriched, and basal-like cancers differed significantly from each other. Furthermore, within the group of luminal tumors Ki-67 values of patients with versus without pCR also differed significantly. Conclusion. Our data shows that the Ki-67 value predicts the response to neoadjuvant chemotherapy as a function of the molecular subtype, reflecting the daily routine concerning Ki-67 and its impressing potential and limitation as a predictive marker for neoadjuvant chemotherapy response.

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“…Moreover, mice are one of the most interesting research models to study the molecular basis of HF due to the availability of many genetically engineered strains made possible by their well-characterized genome and the easy introduction and stable transmission of gene mutations. Moreover, since 99% of the human genes have direct orthologs with mice, it is possible to generate transgenic mice models to mimic human disorders [71,244]. Nevertheless, structural differences regarding human cardiovascular system represent another limitation of rodent models.…”

Section: General Considerationsmentioning

confidence: 99%

Rodent models of heart failure: an updated review

et al. 2012

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Heart failure (HF) is one of the major health and economic burdens worldwide, and its prevalence is continuously increasing. The study of HF requires reliable animal models to study the chronic changes and pharmacologic interventions in myocardial structure and function and to follow its progression toward HF. Indeed, during the past 40 years, basic and translational scientists have used small animal models to understand the pathophysiology of HF and find more efficient ways of preventing and managing patients suffering from congestive HF (CHF). Each species and each animal model has advantages and disadvantages, and the choice of one model over another should take them into account for a good experimental design. The aim of this review is to describe and highlight the advantages and drawbacks of some commonly used HF rodents models, including both non-genetically and genetically engineered models, with a specific subchapter concerning diastolic HF models.

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Microarray analysis to evaluate different animal models for human heart failure

Cited by 10 publications

References 14 publications

Molecular mechanisms in evolutionary cardiology failure

Molecular mechanisms in evolutionary cardiology failure

Can Ki-67 Play a Role in Prediction of Breast Cancer Patients' Response to Neoadjuvant Chemotherapy?

Rodent models of heart failure: an updated review

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