M. C. Islas-Carbajal, A. Rincón-Sánchez, C. A. Nava-Valdivia, C. Charles-Niño
{"title":"The Importance of Autophagy and Proteostasis in Metabolic Cardiomyopathy","authors":"M. C. Islas-Carbajal, A. Rincón-Sánchez, C. A. Nava-Valdivia, C. Charles-Niño","doi":"10.5772/intechopen.92727","DOIUrl":"https://doi.org/10.5772/intechopen.92727","url":null,"abstract":"Metabolic cardiomyopathy and other heart disorders are associated with proteostasis derailment and subsequent autophagy. Proteostasis is a process of protein homeostasis, and autophagy is a mechanism of self-degradation for surviving cells facing stressful conditions. Metabolic challenges have been linked to excess reactive oxygen species. Cardiomyocyte proteotoxicity, an important underlying pathologic mechanism in cardiac disease, is characterized by chronic accumulation of misfolded or unfolded proteins that can lead to proteotoxic formation or aggregation of soluble peptides. Autophagic processes are mediated by the ubiquitin-proteasome and autophagy-lysosome systems, fundamental for cardiac adaptation to physiological and pathological stress. Cellular proteostasis alterations in cardiomyopathy are represented by myocardial remodeling and interstitial fibrosis with reduced diastolic function and arrhythmias. Autophagy regulation may be a potential therapeutic strategy for metabolic cardiomyopathy necessary for the treatment of fibrosis and cardiac tissue remodeling alterations. Furthermore, autophagy has been shown to be active in the perimeter of cardiovascular fibrotic tissue as mechanism of fibrosis recovery and scarring secondary to cell apoptosis. In the present work, we review the current knowledge on the role of autophagy and proteostasis in the pathogenesis of heart failure to resolve the ever-expanding epidemic of metabolic cardiomyopathy and heart failure associated with substantial morbidity and mortality.","PeriodicalId":165821,"journal":{"name":"Cardiovascular Risk Factors in Pathology","volume":"21 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2020-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"117219297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Endothelial Dysfunction and Disruption in Pulmonary Hypertension","authors":"R. Mathew","doi":"10.5772/intechopen.92177","DOIUrl":"https://doi.org/10.5772/intechopen.92177","url":null,"abstract":"A number of systemic diseases lead to pulmonary hypertension (PH), a serious disorder with a high morbidity and mortality rate. Irrespective of the underlying disease, endothelial dysfunction or disruption plays a key role in the initiation and progression of PH. Endothelial dysfunction and disruption result in impaired vascular relaxation response, activation of proliferative pathways leading to medial hypertrophy and PH. Endothelial cells (EC) play a crucial role in regulating vascular tone and maintaining homeostasis. Caveolin-1, a 21-22 kD membrane protein, interacts with a number of transducing factors and maintains them in a negative conformation. Disruption of EC results in endothelial caveolin-1 loss and reciprocal activation of proliferative pathways leading to PH, and the accompanying loss of PECAM1 and vascular endothelial cadherin results in barrier dysfunction. These changes lead to the irreversibility of PH. Hypoxia-induced PH is not accompanied by endothelial disruption or caveolin-1 loss but is associated with caveolin-1 dysfunction and the activation of proliferative pathways. Removal of hypoxic exposure results in the reversal of the disease. Thus, EC integrity is an important factor that determines irreversibility vs. reversibility of PH. This chapter will discuss normal EC function and the differences encountered in PH following EC disruption and EC dysfunction.","PeriodicalId":165821,"journal":{"name":"Cardiovascular Risk Factors in Pathology","volume":"18 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2020-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123419582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Patel, D. Braga, B. Money, Andrés Pirela, A. Zybulewski, B. Olivieri, Robert E. Beasley
{"title":"Pathogenesis of Abdominal Aortic Aneurysm","authors":"M. Patel, D. Braga, B. Money, Andrés Pirela, A. Zybulewski, B. Olivieri, Robert E. Beasley","doi":"10.5772/intechopen.91670","DOIUrl":"https://doi.org/10.5772/intechopen.91670","url":null,"abstract":"Abdominal aortic aneurysms (AAAs) are encountered by many healthcare providers such as interventional radiologists, vascular surgeons, cardiologists, and general practitioners. Much effort has been placed in the screening, diagnosis, and treatment of AAA with somewhat little understanding of its pathophysiology. AAA is a complex disease typically segmented into a process of proteolysis, inflammation, and vascular smooth muscle cell (VSMC) apoptosis with oxidative stress balancing its components. AAA and other aortic syndromes such as aortic dissection share this same process. On the other hand, AAA formation and aortic pathology may be acquired through infection like in mycotic aneurysm or may be genetic in origin such as seen with Ehlers-Danlos and Marfan syndromes.","PeriodicalId":165821,"journal":{"name":"Cardiovascular Risk Factors in Pathology","volume":"78 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2020-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"125026976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Pharmacokinetic Aspects of Statins","authors":"L. Cid-Conde, José López-Castro","doi":"10.5772/intechopen.91910","DOIUrl":"https://doi.org/10.5772/intechopen.91910","url":null,"abstract":"Statins are the most used therapeutic group in the treatment of hypercholesterolemia and reduce the risk of cardiovascular events and mortality. Long prescription periods and their pharmacokinetic characteristics increase the possibility of interactions, especially at the metabolism level. Simvastatin, lovastatin, and atorvastatin are metabolized by CYP3A4 isoenzymes, so they will have more significant interactions than fluvastatin, pitavastatin, and rosuvastatin that require CYP2C9. The main interactions are with macrolides, azole antifungals, antiretrovirals, platelet antiaggregants, anticoagulants, oral antidiabetics, calcium channel blockers, immunosuppressants, and other hypolipidemic agents, among others. A review of all medications that are taken by patients treated with statins should be performed at each medical consultation and during all healthcare transitions.","PeriodicalId":165821,"journal":{"name":"Cardiovascular Risk Factors in Pathology","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2020-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129123869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Statin Therapy in Children","authors":"B. Sunil, A. Ashraf","doi":"10.5772/intechopen.91367","DOIUrl":"https://doi.org/10.5772/intechopen.91367","url":null,"abstract":"Landmark studies such as the Bogalusa Heart study, Pathobiological Determinants of Atherosclerosis in Youth study, and Muscatine and Young Finns studies established that the atherosclerotic process begins in childhood. Early precursors of atherosclerosis may increase risk of cardiovascular morbidity in adulthood. Follow-up studies of children with familial homozygous hypercholesterolemia showed that initiation of statin therapy slowed the progression of carotid intima-media thickness and reduced cardiovascular disease risk. Despite the growing evidence on the efficacy of statins and a rising prevalence of dyslipidemia, there are concerns regarding long-term safety and efficacy. Moreover, data on statin use in children with secondary dyslipidemia are sparse. This chapter provides a comprehensive review of the current state of literature on the indications, contraindications, efficacy and safety data on the use of statins in pediatric dyslipidemia.","PeriodicalId":165821,"journal":{"name":"Cardiovascular Risk Factors in Pathology","volume":"26 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2020-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134543569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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