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Biology of Women’s Heart Health (2023)

Kirshenbaum, Lorrie. [editor.] ; Rabinovich-Nikitin, Inna. [editor.]

Cham :Springer International Publishing :

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Keywords: Cardiovascular system. ; Physiology. ; Cardiology. ; Medicine Research. ; Biology Research. ; Medical sciences. ; Health. ; Sex. ; Cardiovascular Physiology. ; Cardiology. ; Biomedical Research. ; Health Sciences. ; Gender and Health.

Description / Table of Contents: Attenuation of Bnip3 Mediated Doxorubicin-Induced Cell Death in Cardiac Myocytes -- Sex Dependent Regulation of Circadian Rhythms in Health and Disease -- Circadian Pharmacological Approach to Treat Myocardial Infarct -- GPER Function as a Determinant of the Progression of Atherosclerotic Disease in Women -- Novel Therapeutic Approach to Treat Cardiac-Rheumatology in Females -- Correlation between Sex, Immigration Status, Ethnicity, and Long-term Outcomes of Ischemic Stroke -- Risk Assessment and Predictive Modelling for The Heart-Brain Interface in Women -- Insomnia Interventions for Female Cardiac Patients -- Aortic Stenosis Progression, Cardiac Damage, and Survival: Comparison Between Men and Women -- Treatment and Management of Valvular Heart Disease and Cost-Effectiveness Analysis -- Association of Mortality and Acute Aortic Events with Ascending Aortic Aneurysm -- Improving Diagnosis and Treatment for Patients Who Suffer Spontaneous Coronary Artery Dissection (SCAD) -- Preeclampsia and Future Cardiovascular Health -- Cardiovascular Disease in Women with a History of Pregnancy Complications -- Hormone Replacement Treatment for Cardiovascular Disease -- Cardiovascular Mortality Following Early-Stage Breast Cancer -- Lipid Management for the Prevention of Atherosclerotic Cardiovascular Disease in Women -- Sex Differences in Cardiac Rehabilitation Enrollment -- Promoting Exercise and Physical Activity in Female Patients with Heart Disease -- Sex and Gender Differences in the Diagnosis, Treatment, and Outcomes of Coronary Artery Disease -- Sex Differences in Arterial Aging and its Implications on Cardiovascular Diseases -- Impact of a Novel Community-Based Lifestyle Intervention Program on Type 2 Diabetes and Cardiovascular Risk -- Clinical Outcomes Related to Heart Failure and Pulmonary Hypertension -- Examination of Health-Related Quality of Life in Women with Coronary Artery Disease -- The Risks and Benefits of Implantable Cardioverter-Defibrillator Generator Replacement -- The Effects and Roles of Estrogen in Managing Hypertension in Menopausal Women -- The Effects of Menopausal Hormone Therapy on the Vascular System -- Influence of Sex Differences in Non-Obstructive Coronary Artery Disease -- Diet1 and Resistance to High Cholesterol Levels and Cardiovascular Disease -- Interventions to Improve Clinical Outcomes Following Hospitalization for Heart Failure -- Sex-Dependent Cardioprotective Effects of the Phytoestrogen Resveratrol -- Blood Pressure Across a Woman's Life Cycle -- Women’s Fitness Levels and Heart Rate Response to Exercise -- Supervised Exercise Therapy Through Cardiac Rehabilitation following Peripheral Arterial Disease -- Sex Differences in ANT2-Mediated ATP Import into Mitochondria for Protection Against Hypoxia Lethal Injury.

Abstract: Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in women and men worldwide and represents a major financial burden to world health care systems. Importantly, CVD has eclipsed cancer as the leading cause of death for women globally. Through advancements in research and clinical testing, the symptoms and risk factors for CVD have been well established for men, but not for women. Consequently, there is an immediate need for new innovative research that will bridge this gap and allow for improved early diagnosis and treatment of CVD in women. This book will serve as a guide for health care providers to better understand the physiological, biochemical, and genetic differences in heart disease in women with the goal of providing improved education, awareness and treatment of cardiovascular disease in women. The book will cover topics such as: sex dependent clinical outcomes of cardiovascular disease, cardiac protection by estrogen, cardiac health during menopause, cardiac rehabilitation programs, fitness and exercise, cardio-oncology, shift work and the CVD risk, and pregnancy related CVD.

Type of Medium: Online Resource

Pages: VII, 446 p. 56 illus., 38 illus. in color. , online resource.

Edition: 1st ed. 2023.

ISBN: 9783031399282

Series Statement: Advances in Biochemistry in Health and Disease, 26

URL: https://doi.org/10.1007/978-3-031-39928-2

DOI: 10.1007/978-3-031-39928-2

DDC: 573.1

Language: English

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Biochemistry of Apoptosis and Autophagy (2022)

Kirshenbaum, Lorrie A. [editor.]

Cham :Springer International Publishing :

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Keywords: Cytology. ; Cell Biology.

Description / Table of Contents: A Protein-centric Perspective of Autophagy and Apoptosis Signaling and Crosstalk in Health and Disease -- Adrenergic receptor signaling pathways in the regulation of apoptosis -- Apoptosis in Ischemic Heart Disease -- Autophagy in cardiac physiology and pathology -- Caspase signaling pathways as convenors of stress adaptation -- Cross talk between apoptosis and autophagy in regulating the progression of heart disease -- Fibroblasts, Fibrosis and Autophagy -- Gene Therapy and Its Application In Cardiac Diseases -- Inflammation and mitochondrial degradation in the heart -- Mitochondria and Cellular Hosts_An Uneasy Truce -- Mitochondrial Dysfunction and Mitophagy -- Proteotoxicity and Autophagy in Neurodegenerative and Cardiovascular Diseases -- Regulation of Cell Death Signaling Pathways in Cardiac Myocytes by Mitochondrial Bnip3 – Inna -- Role of Cardiomyocyte Apoptosis in Heart Failure -- The Role of FGF2 Isoforms In Cell Survival In The Heart.

Abstract: One of the most intriguing and compelling issues to impact contemporary biology to date is the concept that cell death is genetically regulated. Observations by Kerr and Wyllie, made more than 30 years ago on the basis of distinct morphological criteria, markedly distinguished apoptosis from classical cell death by necrosis. Apoptosis is a highly regulated, evolutionary conserved, genetic program of cell death essential for normal development and tissue homeostasis. The discovery of apoptosis as a regulated event and potentially amenable to therapeutic interventions has generated considerable excitement because it meant that disease entities resulting from either too much, or too little, apoptosis could be potentially cured with new therapies that target apoptosis. While there is little doubt that necrosis induced by massive cellular trauma is likely an unregulated event, several lines of investigation have challenged the dogma that necrotic cell death is merely unregulated. Emerging data has shifted the paradigm in our thinking about necrosis as a regulated event. Autophagy is another cellular process that has received considerable attention over the past two decades and its remarkable involvement in the processes of cell survival, death and tumorigenesis. Macro autophagy is a catabolic process that involves the selective and targeted removal of oxidized proteins, macromolecular structures and organelles through an elaborate cellular process involving a lysosome mediated pathway. Other forms of autophagy involving adapter proteins, commonly referred to as chaperone mediated autophagy, involves the selective removal of cellular cargo by the ubiquitin-proteasome pathway. The book will serve as a reference guide for basic and clinical scientists who are interested in understanding how these critical cellular processes impact the pathogenesis of human disease.

Type of Medium: Online Resource

Pages: XVI, 283 p. 35 illus., 27 illus. in color. , online resource.

Edition: 1st ed. 2022.

ISBN: 9783030787998

Series Statement: Advances in Biochemistry in Health and Disease, 18

URL: https://doi.org/10.1007/978-3-030-78799-8

DOI: 10.1007/978-3-030-78799-8

DDC: 571.6

Language: English

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Adenovirus mediated - gene transfer into cardiomyocytes (1997)

Kirshenbaum, Lorrie A.

Springer

Molecular and cellular biochemistry 172 (1997), S. 13-21

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ISSN: 1573-4919

Keywords: adenovirus ; ventricular myocytes ; DNA synthesis ; cell cycle

Source: Springer Online Journal Archives 1860-2000

Topics: Biology , Chemistry and Pharmacology , Medicine

Notes: Abstract To circumvent limitations imposed by conventional gene transfer techniques into cardiac muscle cells, we studied whether replication defective adenovirus would obviate this limitation to basic studies of signal transduction and transcriptional control processes in the heart. We demonstrate here the utility of adenovirus mediated gene transfer to introduce foreign DNA into post-mitotic terminally differentiated ventricular myocytes with uniformity and high efficiency. We also provide evidence for the genetic modification of neonatal ventricular myocytes by adenovirus early region 1 (E1) proteins and their impact on cardiac gene transcription and DNA synthesis respectively. Thus, for studies of transcriptional control processes in the heart, which until now have been restricted to neonatal ventricular myocytes; adenovirus mediated gene transfer provides a means to genetically manipulate adult cardiac muscle cells. The advent of adenovirus gene transfer will extend our understanding of the molecular mechanisms that mediate basic cardiac disease and may ultimately provide a means to therapeutically mitigate the disease process.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1023/A:1006853824044

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Control of cardiac gene transcription by fibroblast growth factors (1994)

Schneider, Michael D. ; Kirshenbaum, Lorrie A. ; Brand, Thomas ; [et al.]

New York, NY [u.a.] : Wiley-Blackwell

Molecular Reproduction and Development 39 (1994), S. 112-117

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ISSN: 1040-452X

Keywords: Actin ; Adenovirus ; Dominant-negative receptors ; Serum response factor ; Transcription factors ; Life and Medical Sciences ; Cell & Developmental Biology

Source: Wiley InterScience Backfile Collection 1832-2000

Topics: Biology

Notes: Skeletal α-actin (SkA) is representative of the cardiac genes that are expressed at high levels in embryonic myocardium, downregulated after birth, and reactivated by trophic signals including basic fibroblast growth factor (FGF-2) and type β transforming growth factors (TGFβ). To investigate the molecular basis for cardiac-restricted and growth factor-induced SkA transcription, we have undertaken a mutational analysis of the SkA promoter in neonatal ventricular myocytes, with emphasis on the role of three nominal serum response elements. Serum response factor (SRF) and the bifunctional factor YY1 are the predominant cardiac proteins contacting the proximal SRE (SRE1). Mutations of SRE1 that prevent recognition by SRF and YY1, or SRF alone, virtually abolish SkA transcription; mutation of distal SREs was ineffective. A mutation which selectively abrogates YY1 binding increases expression, substantiating the predicted role of YY1 as an inhibitor of SRF effects. SkA transcription requires combinatorial action of SRE1 with consensus sites for Sp1 and the SV40 enhancer binding protein, TEF-1. As an isolated motif, SRE1 can confer responsiveness to both FGF-2 and TGFβ to a heterologous promoter. Whether TEF-1 binding sites likewise can function as FGF response elements is unknown.Molecular dissection of mechanisms that govern the differentiated cardiac phenotype has largely been undertaken to date in neonatal ventricular myocytes, as the adult ventricular myocyte has been refractory to conventional procedures for gene transfer. To circumvent expected limitations of other methods, we have used replication-deficient adenovirus to achieve efficient gene transfer to adult cardiac cells in culture. Adult rat ventricular myocytes were infected, 24 h after plating, with adenovirus type 5 containing a CMV-IE promoter-driven lacZ reporter gene, and were assayed for the presence of β-galactosidase 48 h after infection. The frequency of lacZ+ rod-shaped myocytes was half-maximal at 4 ×105 PFU, and approached 90% at 1 × 108 PFU. Uninfected cells and cells infected with lacZ- virus remained colorless. The β-galactosidase activity concurred with the proportion of lacZ+ cells and was contingent on the presence of exogenous lacZ gene. Thus, adult ventricular myocytes are amenable to efficient gene transfer with recombinant adenovirus.We have constructed virus conferring luciferase activity driven by the SkA promoter (Ad5/SkA/luc) to test for potential developmental control of growth factor responses in cardiac muscle. In adult ventricular myocytes, the construct remains inducible by TGFβ, but little or no response is seen to FGF-2 or FGF-1, which is consistent with prior reports that the FGF receptor is downregulated in terminally differentiated ventricular muscle cells. The relative uniformity for gene transfer by adenovirus should facilitate tests to determine the impact of FGF receptors and FGF signaling proteins upon the endogenous genes and gene products of virally modified adult ventricular muscle cells. © 1994 Wiley-Liss, Inc.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1002/mrd.1080390117

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