Gender Differences of Cardiovascular Disease

Meyer, Matthias R.; Haas, Elvira; Barton, Matthias

doi:10.1161/01.hyp.0000223064.62762.0b

Cited by 136 publications

(86 citation statements)

References 112 publications

(103 reference statements)

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“…The binding triggers or inhibits the transcription of certain genes being responsive to estrogens. Besides, estrogen-ER complex may interact with transcription factors, such as SP-1 (Meyer et al, 2006). So, ER targeting could be an approach of both chemoprevention and cancer targeted therapy (Manni et al, 2011).…”

Section: Estrogenic Effects Of Citrus Flavonoidsmentioning

confidence: 99%

“…Interactions of estrogen and ER affect the expression of HDL and LDL receptors, resulting in the increasing of HDL and decreasing of LDL level, thus play a role in cholesterol modulation (Meyer et al, 2006), whilst estrogen's role in maintaining bone density occurs through its ability to increase the activity of osteoblast and suppress the activity of osteoclast. The binding of estrogen to ER also may activate certain transcription factors, such as c-Myc, that later transcripts genes resulting in the activation of cell cycle.…”

Section: Estrogenic Effects Of Citrus Flavonoidsmentioning

confidence: 99%

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Natural Products for Cancer-Targeted Therapy: Citrus Flavonoids as Potent Chemopreventive Agents

Meiyanto

Hermawan²

2012

Asian Pacific Journal of Cancer Prevention

211

135

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One example is hesperidin having the ability to decrease the concentration of serum and hepatic lipid and reduce osteoporosis of ovariectomized rats. Those studies showed the great potential of citrus fruits as natural product to be developed as not only the source of co-chemotherapeutic agents, but also phyto-estrogens. Therefore, further study needs to be conducted to explore the potential of citrus fruits in overcoming cancer

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Section: Estrogenic Effects Of Citrus Flavonoidsmentioning

confidence: 99%

Section: Estrogenic Effects Of Citrus Flavonoidsmentioning

confidence: 99%

Natural Products for Cancer-Targeted Therapy: Citrus Flavonoids as Potent Chemopreventive Agents

Meiyanto

Hermawan²

2012

Asian Pacific Journal of Cancer Prevention

211

135

View full text Add to dashboard Cite

show abstract

“…Endogenous estrogens are powerful antioxidants, which inhibit the generation of reactive oxygen species and increase the bioavailability of nitric oxide. 31 Thus, it is possible that eNOS reduction by estrogen deficiency may augment AC-induced inflammation not only directly but also indirectly by chronically increasing superoxide generation. A combination of pressure overload and eNOS reduction may have activated unknown mechanisms to augment inflammation and myocardial fibrosis in OVX+AC rats.…”

Section: E2 Deficiency and Diastolic Dysfunctionmentioning

confidence: 99%

Enhanced cardiac inflammation and fibrosis in ovariectomized hypertensive rats: a possible mechanism of diastolic dysfunction in postmenopausal women

et al. 2011

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Diastolic dysfunction is more prevalent in individuals with hypertension, particularly postmenopausal women; however, the pathogenesis of diastolic dysfunction remains unknown. Pressure overload activates cardiac inflammation, which induces myocardial fibrosis and diastolic dysfunction in rats with a suprarenal aortic constriction (AC). Therefore, we examined the effects of bilateral ovariectomy (OVX) on left ventricle (LV) remodeling, diastolic dysfunction and cardiac inflammation in hypertensive female rats. Rats were randomized to OVX+AC, OVX and AC groups as well as a Control group receiving sham operations for both the procedures. Rats underwent OVX at 6 weeks and AC at 10 weeks (Day 0). At Day 28, OVX did not appear to affect arterial pressure, cardiac hypertrophy or LV fractional shortening in AC rats. However, OVX increased myocardial fibrosis, elevated LV end-diastolic pressure and reduced the transmitral Doppler spectra early to late filling velocity ratio in AC rats. AC-induced transient myocardial monocyte chemoattractant protein-1 expression and macrophage infiltration, both of which peaked at Day 3 and were augmented and prolonged by OVX. At Day 28, dihydroethidium staining revealed superoxide generation in the intramyocardial arterioles in the OVX+AC group but not in the AC group. NOX1, a functional subunit of nicotinamide adenine dinucleotide phosphate oxidase, was upregulated only in the OVX+AC group at Day 28. Chronic 17b-estradiol replacement prevented the increases in macrophage infiltration, NOX1 upregulation, myocardial fibrosis and diastolic dysfunction in OVX+AC rats. In conclusion, we suggest that estrogen deficiency augments cardiac inflammation and oxidative stress and thereby aggravates myocardial fibrosis and diastolic dysfunction in hypertensive female rats. The findings provide insight into the mechanism underlying diastolic dysfunction in hypertensive postmenopausal women. Hypertension Research (2011) 34, 496-502; doi:10.1038/hr.2010; published online 20 January 2011Keywords: estradiol; gender medicine; macrophage; myocardial fibrosis; oxidative stress INTRODUCTIONThe ejection fraction of the left ventricle (LV) is normal in approximately half of all patients with congestive heart failure, which indicates that impaired diastolic function in these patients is the major cause of heart failure. [1][2][3] Hypertension is the most common coexisting disease in patients with diastolic heart failure. Diastolic heart failure is more prevalent in women than in men, especially in postmenopausal hypertensive women, which may be due to decreased estrogen levels. 2,3 Determinants of diastolic function include active myocardial relaxation and passive properties of the LV wall. 2 Sequestration of calcium and cross-bridge uncoupling after systole are involved in the active process of relaxation. Previous studies have shown that estrogen

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“…Although obesity is rising in prevalence and incidence in the United States, not all obese individuals are at equal risk for obesity-induced cardiovascular and metabolic diseases. For example, reproductive aged women are relatively protected from cardiovascular disease compared with age-matched men (1). Estrogen receptor signaling probably contributes to many of these effects, but because estrogen replacement therapy alone is not sufficient to improve health, other mechanisms are likely involved (2).…”

mentioning

confidence: 99%

Differences in Hematopoietic Stem Cells Contribute to Sexually Dimorphic Inflammatory Responses to High Fat Diet-induced Obesity

Singer

Maley

Mergian

et al. 2015

Journal of Biological Chemistry

103

120

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Background: Diet-induced obesity leads to a chronic low grade inflammation with production of activated macrophages associated with systemic sexually dimorphic metabolic dysfunction. Results: Males have enhanced myelopoiesis and a proinflammatory response to obesity compared with females. Conclusion: Sex differences in myelopoiesis result in dimorphic responses to obesity-induced inflammation. Significance: Given differences in inflammatory responses, targeted treatment strategies are probably required for males and females.

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Gender Differences of Cardiovascular Disease

Cited by 136 publications

References 112 publications

Natural Products for Cancer-Targeted Therapy: Citrus Flavonoids as Potent Chemopreventive Agents

Natural Products for Cancer-Targeted Therapy: Citrus Flavonoids as Potent Chemopreventive Agents

Enhanced cardiac inflammation and fibrosis in ovariectomized hypertensive rats: a possible mechanism of diastolic dysfunction in postmenopausal women

Differences in Hematopoietic Stem Cells Contribute to Sexually Dimorphic Inflammatory Responses to High Fat Diet-induced Obesity

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