Serotonin and Cardiovascular Diseases

Monassier, Laurent; Maroteaux, Luc

doi:10.1016/b978-0-12-800050-2.00012-7

Cited by 10 publications

(3 citation statements)

References 160 publications

(173 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Due to their participation in the physiological and pathological processes in the cardiovascular system, 5-HT2 receptors are of great therapeutic relevance. In addition to being present in various areas of the CNS, 5-HT2A receptors [73] are observed on the cell membrane of platelets [74], smooth muscle cells [75], and cardiomyocytes along with 5-HT2B receptors [15,76]. 5-HT accumulates in the myocardial interstitium and plays an important role in the progression of myocardial cellular injury through various pathways utilizing 5-HT2A and 5-HT2B receptors along with uptake transporters of 5-HT [10,[13][14][15].…”

Section: Discussionmentioning

confidence: 99%

Cardioprotective Effect of Flibanserin against Isoproterenol-Induced Myocardial Infarction in Female Rats: Role of Cardiac 5-HT2A Receptor Gene/5-HT/Ca2+ Pathway

et al. 2023

View full text Add to dashboard Cite

Myocardial infarction (MI) is a life-threatening ischemic disease and is one of the leading causes of morbidity and mortality worldwide. Serotonin (5-HT) release during myocardial ischemia plays an important role in the progression of myocardial cellular injury. This study was conducted to investigate the possible cardioprotective effect of flibanserin (FLP) against isoproterenol (ISO)-induced MI in rats. Rats were randomly divided into five groups and were treated orally (p.o.) with FLP (15, 30, and 45 mg/kg) for 28 days. ISO was administered subcutaneously (S.C.) (85 mg/kg) on the 27th and 28th days to induce MI. ISO-induced myocardial infarcted rats exhibited a significant increase in cardiac markers, oxidative stress markers, cardiac and serum 5-HT levels, and total cardiac calcium (Ca2+) concentration. ISO-induced myocardial infarcted rats also revealed a remarkable alteration of electrocardiogram (ECG) pattern and significantly upregulated expression of the 5-Hydroxytryptamine 2A (5-HT2A) receptors gene. Moreover, ISO-induced myocardial infarcted rats showed significant histopathological findings of MI and hypertrophic signs. However, pretreatment with FLP significantly attenuated the ISO-induced MI in a dose-dependent manner, as the effect of FLP (45 mg/kg) was more pronounced than that of the other two doses, FLP (15 and 30 mg/kg). The present study provides evidence for the cardioprotective efficacy of FLP against ISO-induced MI in rats.

show abstract

Section: Discussionmentioning

confidence: 99%

Cardioprotective Effect of Flibanserin against Isoproterenol-Induced Myocardial Infarction in Female Rats: Role of Cardiac 5-HT2A Receptor Gene/5-HT/Ca2+ Pathway

et al. 2023

View full text Add to dashboard Cite

show abstract

“…Serotonin (SRT) is a hormone well known for its activity in the central nervous system. Its biosynthesis takes place in the nervous system, it is also accumulated in thrombocytes [115]. SRT, similar to ET-1, has vasoconstrictive effects in dogs [116][117][118][119].…”

Section: Serotoninmentioning

confidence: 99%

Pulmonary Hypertension Secondary to Myxomatous Mitral Valve Disease in Dogs: Current Insights into the Histological Manifestation and Its Determining Factors

Grzeczka,

Pasławska,

Graczyk

et al. 2024

Applied Sciences

View full text Add to dashboard Cite

Pulmonary venous hypertension (PVH) is caused by deteriorating left ventricular function. The most common cause of PVH in dogs is myxomatous mitral valve degeneration (MMVD). It causes left ventricular volume overload and an increase in left atrial and pulmonary venous pressure (PVH), which leads to pulmonary vascular wall remodeling and contributes to the perpetuation and worsening of PVH. Pulmonary vascular wall remodeling is also characteristic of pulmonary arterial hypertension (PAH). However, the changes in PVH arise secondary to heart failure and vascular remodeling progresses as the disease progresses. On the other hand, PAH is a primary disease that can be triggered, for example, by the use of certain drugs. Similar structural changes may suggest the influence of similar pathophysiological mechanisms or the intermediation of similar mediators. Therefore, this article discusses recent and hitherto uncommented findings elucidating the pathophysiology of the processes and influences on the pattern of histological changes observed in pulmonary hypertension secondary to degenerative mitral valve disease. In particular, we focus on the activity of factors such as endothelin, serotonin, and nitric oxide, which are involved in pulmonary vascular wall remodeling in both PVH and PAH.

show abstract

“…Serotonin is secreted by enterochromaffin cells of the digestive tract and stored in platelets. This circulating stock may be captured by sympathetic neurons and endothelial cells [ 113 ]. It has been theorized that circulating serotonin may play a role in systemic arterial hypertension [ 114 ] and high circulating serotonin has been reported to be a risk factor for coronary artery disease, particularly in younger age groups [ 115 ].…”

Section: Biomarkers Of Stress and The Biology Of Adversitymentioning

confidence: 99%

By what molecular mechanisms do social determinants impact cardiometabolic risk?

et al. 2023

View full text Add to dashboard Cite

While it is well known from numerous epidemiologic investigations that social determinants (socioeconomic, environmental, and psychosocial factors exposed to over the life-course) can dramatically impact cardiovascular health, the molecular mechanisms by which social determinants lead to poor cardiometabolic outcomes are not well understood. This review comprehensively summarizes a variety of current topics surrounding the biological effects of adverse social determinants (i.e., the biology of adversity), linking translational and laboratory studies with epidemiologic findings. With a strong focus on the biological effects of chronic stress, we highlight an array of studies on molecular and immunological signaling in the context of social determinants of health (SDoH). The main topics covered include biomarkers of sympathetic nervous system and hypothalamic–pituitary–adrenal axis activation, and the role of inflammation in the biology of adversity focusing on glucocorticoid resistance and key inflammatory cytokines linked to psychosocial and environmental stressors (PSES). We then further discuss the effect of SDoH on immune cell distribution and characterization by subset, receptor expression, and function. Lastly, we describe epigenetic regulation of the chronic stress response and effects of SDoH on telomere length and aging. Ultimately, we highlight critical knowledge gaps for future research as we strive to develop more targeted interventions that account for SDoH to improve cardiometabolic health for at-risk, vulnerable populations.

show abstract

Serotonin and Cardiovascular Diseases

Cited by 10 publications

References 160 publications

Cardioprotective Effect of Flibanserin against Isoproterenol-Induced Myocardial Infarction in Female Rats: Role of Cardiac 5-HT2A Receptor Gene/5-HT/Ca2+ Pathway

Cardioprotective Effect of Flibanserin against Isoproterenol-Induced Myocardial Infarction in Female Rats: Role of Cardiac 5-HT2A Receptor Gene/5-HT/Ca2+ Pathway

Pulmonary Hypertension Secondary to Myxomatous Mitral Valve Disease in Dogs: Current Insights into the Histological Manifestation and Its Determining Factors

By what molecular mechanisms do social determinants impact cardiometabolic risk?

Contact Info

Product

Resources

About