Pub Date : 2016-09-12DOI: 10.1080/17584299.2016.1230316
V. Athyros, K. Imprialos, M. Doumas, A. Karagiannis
Sodium/glucose co-transporter 2 inhibitors (SGLT2i) lower blood glucose by inhibiting the reabsorption of glucose in the proximal renal tubules.[1] There are several licensed SGLT2i. One of them, empagliflozin, was evaluated in the EMPA-REG OUTCOME trial.[2] This prospective, randomised, double-blind, placebo-controlled, survival study included 7020 patients with type 2 diabetes mellitus (T2DM) and followed them for a median period of 3.1 years.[2] The EMPAREG OUTCOME trial showed that the use of either 10 or 25 mg/d of empagliflozin (cumulative results presentation because there were no significant differences between the two doses) on top of standard therapy produced relative risk reductions in the primary endpoint [cumulative incidence of death from cardiovascular disease (CVD), nonfatal myocardial infarction (MI) or nonfatal stroke] by 14%, total mortality by 32%, of CVD mortality by 38% and hospitalisation for heart failure (HF) by 35% compared with placebo; all reductions were highly statistically significant.[2] The main side effect was an increased rate of genital infection.[2] Following a review of a few cases, the European Medical Agency recommended an update of all SGLT2i Summary of Product Characteristics to include diabetic ketoacidosis as a rare of (1/1000 patients) adverse reaction (http:// www.ema.europa.eu/ema/index.jsp?curl=pages/medicines/human/referrals/SGLT2_inhibitors/humanreferral_ prac000052.jsp&mid=WC0b01ac05805c516f ). The EMPA-REG OUTCOME trial results were a surprise; the Evaluation of Cardiovascular Outcome Results (LEADER) trial with liraglutide, a human glucagon like peptide 1 receptors agonist (GLP1 RA), that showed similar clinical benefits in terms of improved survival, except for the reduction in hospitalisation for HF, were presented a few months later.[3] The mechanisms driving the effects of empagliflozin on HF and CVD death are not clear.[4] Potential mechanisms include osmotic diuresis, modulation of the cardiorenal axis that reduced plasma volume and less sodium retention, reduction in arterial stiffness, reduced left ventricular afterload, fall in body weight and blood pressure (BP), without increases in sympathetic nervous activity, delay in renal function impairment, reduction in hyperglycaemia with linked reduction in insulin levels and reductions in serum uric acid (SUA) levels.[4,5] However, even all those collectively may not be enough to explain the substantial clinical benefits of empagliflozin manifested early (within the first 3 months of the study) in the EMPA-REG trial.[2] Recently, two papers tried to explain the possible mechanism of empagliflozin clinical benefits focusing on its effect on heart metabolism or “energetics”; this hypothesis, together with all the off-target effects mentioned above, might be an explanation for the beneficial outcomes of empagliflozin in the EMPA-REG trial.[6,7] Several years ago, it was suggested that people with T2DM or insulin resistance have an impaired myo
{"title":"Beneficial effects of sodium glucose co-transporter 2 inhibitors (SGLT2i) on heart failure and cardiovascular death in patients with type 2 diabetes might be due to their off-target effects on cardiac metabolism","authors":"V. Athyros, K. Imprialos, M. Doumas, A. Karagiannis","doi":"10.1080/17584299.2016.1230316","DOIUrl":"https://doi.org/10.1080/17584299.2016.1230316","url":null,"abstract":"Sodium/glucose co-transporter 2 inhibitors (SGLT2i) lower blood glucose by inhibiting the reabsorption of glucose in the proximal renal tubules.[1] There are several licensed SGLT2i. One of them, empagliflozin, was evaluated in the EMPA-REG OUTCOME trial.[2] This prospective, randomised, double-blind, placebo-controlled, survival study included 7020 patients with type 2 diabetes mellitus (T2DM) and followed them for a median period of 3.1 years.[2] The EMPAREG OUTCOME trial showed that the use of either 10 or 25 mg/d of empagliflozin (cumulative results presentation because there were no significant differences between the two doses) on top of standard therapy produced relative risk reductions in the primary endpoint [cumulative incidence of death from cardiovascular disease (CVD), nonfatal myocardial infarction (MI) or nonfatal stroke] by 14%, total mortality by 32%, of CVD mortality by 38% and hospitalisation for heart failure (HF) by 35% compared with placebo; all reductions were highly statistically significant.[2] The main side effect was an increased rate of genital infection.[2] Following a review of a few cases, the European Medical Agency recommended an update of all SGLT2i Summary of Product Characteristics to include diabetic ketoacidosis as a rare of (1/1000 patients) adverse reaction (http:// www.ema.europa.eu/ema/index.jsp?curl=pages/medicines/human/referrals/SGLT2_inhibitors/humanreferral_ prac000052.jsp&mid=WC0b01ac05805c516f ). The EMPA-REG OUTCOME trial results were a surprise; the Evaluation of Cardiovascular Outcome Results (LEADER) trial with liraglutide, a human glucagon like peptide 1 receptors agonist (GLP1 RA), that showed similar clinical benefits in terms of improved survival, except for the reduction in hospitalisation for HF, were presented a few months later.[3] The mechanisms driving the effects of empagliflozin on HF and CVD death are not clear.[4] Potential mechanisms include osmotic diuresis, modulation of the cardiorenal axis that reduced plasma volume and less sodium retention, reduction in arterial stiffness, reduced left ventricular afterload, fall in body weight and blood pressure (BP), without increases in sympathetic nervous activity, delay in renal function impairment, reduction in hyperglycaemia with linked reduction in insulin levels and reductions in serum uric acid (SUA) levels.[4,5] However, even all those collectively may not be enough to explain the substantial clinical benefits of empagliflozin manifested early (within the first 3 months of the study) in the EMPA-REG trial.[2] Recently, two papers tried to explain the possible mechanism of empagliflozin clinical benefits focusing on its effect on heart metabolism or “energetics”; this hypothesis, together with all the off-target effects mentioned above, might be an explanation for the beneficial outcomes of empagliflozin in the EMPA-REG trial.[6,7] Several years ago, it was suggested that people with T2DM or insulin resistance have an impaired myo","PeriodicalId":55252,"journal":{"name":"Clinical Lipidology","volume":"101 1","pages":"2 - 5"},"PeriodicalIF":0.0,"publicationDate":"2016-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76767727","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}
Abstract Numerous clinical studies with objectives such as mortality and morbidity of cardiovascular (CV) have reported the benefit of treatment for dyslipidemia with lipid-lowering therapy, in particular using the statins. But the trials conducted in past years did not consider the gender differences of statin effect, because women were poorly represented. All the results in terms of response, efficacy, reduction of LDL cholesterol and CV risk in primary and secondary prevention refer to men. In these recent years, it emerges the need to consider the different lipoprotein profile during lifetime and CV risk between men and women. Furthermore it is necessary to consider that, in patients with coronary artery disease, the lipid goal achieved is different between the two genders. Finally, we have to evaluate the side effects mostly present in women. In conclusion, there is a different prescription of these treatments in particular in the dosage used, that it is insufficient in women with cardiovascular disease. More recently it has emerged the exigency to use new guidelines that clearly indicate how should be the medical care, therefore, the specific way to treat men and women.
{"title":"Considering gender in prescribing statins: what do physicians need to know?","authors":"C. Pavanello, Giuliana Mombelli","doi":"10.2217/clp.15.39","DOIUrl":"https://doi.org/10.2217/clp.15.39","url":null,"abstract":"Abstract Numerous clinical studies with objectives such as mortality and morbidity of cardiovascular (CV) have reported the benefit of treatment for dyslipidemia with lipid-lowering therapy, in particular using the statins. But the trials conducted in past years did not consider the gender differences of statin effect, because women were poorly represented. All the results in terms of response, efficacy, reduction of LDL cholesterol and CV risk in primary and secondary prevention refer to men. In these recent years, it emerges the need to consider the different lipoprotein profile during lifetime and CV risk between men and women. Furthermore it is necessary to consider that, in patients with coronary artery disease, the lipid goal achieved is different between the two genders. Finally, we have to evaluate the side effects mostly present in women. In conclusion, there is a different prescription of these treatments in particular in the dosage used, that it is insufficient in women with cardiovascular disease. More recently it has emerged the exigency to use new guidelines that clearly indicate how should be the medical care, therefore, the specific way to treat men and women.","PeriodicalId":55252,"journal":{"name":"Clinical Lipidology","volume":"1 5","pages":"499 - 512"},"PeriodicalIF":0.0,"publicationDate":"2015-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/clp.15.39","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72485268","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}
I. Miñambres, J. L. Sánchez-Quesada, Antonio Pérez
Abstract The metabolic syndrome and its components have been associated with hypovitaminosis D in many observational trials. Several mechanisms have been proposed to explain this relationship and include most conditions that are present in patients with the metabolic syndrome. A causal relationship of the association between the metabolic syndrome and hypovitaminosis D, however, has not been demonstrated, and the cardiovascular and metabolic benefits of vitamin D supplementation have not been confirmed. For the time being therefore, supplementation with vitamin D should only be recommended to maintain bone health and to avoid falls.
{"title":"The association between hypovitaminosis D and metabolic syndrome: current understanding","authors":"I. Miñambres, J. L. Sánchez-Quesada, Antonio Pérez","doi":"10.2217/clp.15.38","DOIUrl":"https://doi.org/10.2217/clp.15.38","url":null,"abstract":"Abstract The metabolic syndrome and its components have been associated with hypovitaminosis D in many observational trials. Several mechanisms have been proposed to explain this relationship and include most conditions that are present in patients with the metabolic syndrome. A causal relationship of the association between the metabolic syndrome and hypovitaminosis D, however, has not been demonstrated, and the cardiovascular and metabolic benefits of vitamin D supplementation have not been confirmed. For the time being therefore, supplementation with vitamin D should only be recommended to maintain bone health and to avoid falls.","PeriodicalId":55252,"journal":{"name":"Clinical Lipidology","volume":"35 1","pages":"513 - 524"},"PeriodicalIF":0.0,"publicationDate":"2015-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81333952","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}
Pub Date : 2015-12-01Epub Date: 2015-11-23DOI: 10.2217/clp.15.37
Marco Gentile, Ilenia Calcaterra, Alfonso Strazzullo, Carmen Pagano, Delia Pacioni, Enza Speranza, Paolo Rubba, Gennaro Marotta
Aim: The aim of this study was to test small dense LDL changes with Armolipid Plus treatment in patients with familial combined hyperlipidemia (FCHL).
Methods: After 4 weeks, 30 patients with FCHL were included in an 8-week, randomized, double-blind study and were taking, in addition to the standard diet, either placebo or Armolipid Plus.
Results: The placebo group showed no statistically significant differences in the studied parameters; instead, in the Armolipid Plus group, statistically significant reduction differences were detected in BMI (p = 0.010), LDL score (p = 0.035) and an increase in mean LDL particle diameter (p = 0.040).
Conclusion: The combination of a standard diet with Armolipid Plus is able to reduce LDL score and increase LDL particle diameter in a group of FCHL after 8 weeks of treatment.
{"title":"Effects of Armolipid Plus on small dense LDL particles in a sample of patients affected by familial combined hyperlipidemia.","authors":"Marco Gentile, Ilenia Calcaterra, Alfonso Strazzullo, Carmen Pagano, Delia Pacioni, Enza Speranza, Paolo Rubba, Gennaro Marotta","doi":"10.2217/clp.15.37","DOIUrl":"10.2217/clp.15.37","url":null,"abstract":"<p><strong>Aim: </strong>The aim of this study was to test small dense LDL changes with Armolipid Plus treatment in patients with familial combined hyperlipidemia (FCHL).</p><p><strong>Methods: </strong>After 4 weeks, 30 patients with FCHL were included in an 8-week, randomized, double-blind study and were taking, in addition to the standard diet, either placebo or Armolipid Plus.</p><p><strong>Results: </strong>The placebo group showed no statistically significant differences in the studied parameters; instead, in the Armolipid Plus group, statistically significant reduction differences were detected in BMI (p = 0.010), LDL score (p = 0.035) and an increase in mean LDL particle diameter (p = 0.040).</p><p><strong>Conclusion: </strong>The combination of a standard diet with Armolipid Plus is able to reduce LDL score and increase LDL particle diameter in a group of FCHL after 8 weeks of treatment.</p>","PeriodicalId":55252,"journal":{"name":"Clinical Lipidology","volume":"10 6","pages":"475-480"},"PeriodicalIF":0.0,"publicationDate":"2015-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4821502/pdf/nihms-742001.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34391466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Abstract Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality worldwide. Dyslipidemia is a major risk factor, with elevated plasma lipids having a well-established relationship with CVD. While lifestyle modification and statins have played an important role in reducing risk, many patients develop CVD despite best care. Statins remain the most prescribed lipid-lowering therapy, yet many patients may require additional therapies. Fibrates, ezetimibe and bile acid sequestrants have been extensively investigated thus far, with mixed results. Newer classes of lipid modifying therapy include monoclonal antibodies to PCSK9, lomitapide and cholesterol ester transfer protein inhibitors. In this review, we revisit the history of lipid-lowering therapy, the pharmacotherapies currently used and future direction of research.
{"title":"The past, present and future of lipidlowering therapy","authors":"Osman Najam, G. Lambert, K. Ray","doi":"10.2217/clp.15.40","DOIUrl":"https://doi.org/10.2217/clp.15.40","url":null,"abstract":"Abstract Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality worldwide. Dyslipidemia is a major risk factor, with elevated plasma lipids having a well-established relationship with CVD. While lifestyle modification and statins have played an important role in reducing risk, many patients develop CVD despite best care. Statins remain the most prescribed lipid-lowering therapy, yet many patients may require additional therapies. Fibrates, ezetimibe and bile acid sequestrants have been extensively investigated thus far, with mixed results. Newer classes of lipid modifying therapy include monoclonal antibodies to PCSK9, lomitapide and cholesterol ester transfer protein inhibitors. In this review, we revisit the history of lipid-lowering therapy, the pharmacotherapies currently used and future direction of research.","PeriodicalId":55252,"journal":{"name":"Clinical Lipidology","volume":"43 1","pages":"481 - 498"},"PeriodicalIF":0.0,"publicationDate":"2015-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76317918","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}
Abstract Ischemic heart disease is the leading cause of death worldwide, accounting for approximately 11% of all deaths in 2011. Numerous studies have shown that cardiovascular risk correlates positively and powerfully with total or LDL-cholesterol (LDL-C) and correlates inversely with HDl-cholesterol (HDL-C). Much effort has spent comparing proatherogenic cholesterol markers LDL-C, non-HDL-C, apoB and LDL particle number, while little effort has been spent comparing the markers of the antiatherogenic marker apoA-I and HDL-C. Therefore, this review focused on comparing apoA-I and HDL-C in the prediction of heart disease and myocardial infarction. We identified 28 studies of which 12 indicated that the HDL-C was likely to be a superior marker of risk for heart disease and myocardial infarction compared with eight studies that identified apoA-I to be a superior marker of risk.
{"title":"The value of apoA-I in predicting heart disease and myocardial infarction","authors":"C. Schmidt, G. Bergström, A. Sniderman","doi":"10.2217/clp.15.36","DOIUrl":"https://doi.org/10.2217/clp.15.36","url":null,"abstract":"Abstract Ischemic heart disease is the leading cause of death worldwide, accounting for approximately 11% of all deaths in 2011. Numerous studies have shown that cardiovascular risk correlates positively and powerfully with total or LDL-cholesterol (LDL-C) and correlates inversely with HDl-cholesterol (HDL-C). Much effort has spent comparing proatherogenic cholesterol markers LDL-C, non-HDL-C, apoB and LDL particle number, while little effort has been spent comparing the markers of the antiatherogenic marker apoA-I and HDL-C. Therefore, this review focused on comparing apoA-I and HDL-C in the prediction of heart disease and myocardial infarction. We identified 28 studies of which 12 indicated that the HDL-C was likely to be a superior marker of risk for heart disease and myocardial infarction compared with eight studies that identified apoA-I to be a superior marker of risk.","PeriodicalId":55252,"journal":{"name":"Clinical Lipidology","volume":"13 1","pages":"525 - 541"},"PeriodicalIF":0.0,"publicationDate":"2015-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87396389","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}
Abstract “the ability of the apoA-I mimetic peptides (as demonstrated by 6F) to modulate formation or block activity of unsaturated lysophosphatidic acid in the gut appears to the relevant mechanism of action for atheroprevention.” Submitted: 5 August 2015; Accepted: 14 August 2015; Online: 23 November 2015
{"title":"Apolipoprotein A-I mimetic peptides in dyslipidemia and atherosclerosis: an investigational timeline","authors":"G. Wool","doi":"10.2217/clp.15.35","DOIUrl":"https://doi.org/10.2217/clp.15.35","url":null,"abstract":"Abstract “the ability of the apoA-I mimetic peptides (as demonstrated by 6F) to modulate formation or block activity of unsaturated lysophosphatidic acid in the gut appears to the relevant mechanism of action for atheroprevention.” Submitted: 5 August 2015; Accepted: 14 August 2015; Online: 23 November 2015","PeriodicalId":55252,"journal":{"name":"Clinical Lipidology","volume":"39 1","pages":"467 - 473"},"PeriodicalIF":0.0,"publicationDate":"2015-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77038332","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}
Abstract Familial hypercholesterolemia (FH) is the most common single gene disorder of lipid metabolism. Identifying the genetic cause of FH affects the management of the patient and their family members. Traditional genetic testing methods have been limited by throughput and cost, and therefore the majority of patients have not received a molecular diagnosis. Genetic testing technology has made huge advances in recent years, and these advances are now being translated to improve clinical diagnostic testing for many genetic disorders including FH. This review describes these advances in genetic testing, and considers their implications for the diagnosis and treatment of FH.
{"title":"The past, present and future of molecular genetic diagnosis in familial hypercholesterolemia","authors":"E. Thomas","doi":"10.2217/clp.15.29","DOIUrl":"https://doi.org/10.2217/clp.15.29","url":null,"abstract":"Abstract Familial hypercholesterolemia (FH) is the most common single gene disorder of lipid metabolism. Identifying the genetic cause of FH affects the management of the patient and their family members. Traditional genetic testing methods have been limited by throughput and cost, and therefore the majority of patients have not received a molecular diagnosis. Genetic testing technology has made huge advances in recent years, and these advances are now being translated to improve clinical diagnostic testing for many genetic disorders including FH. This review describes these advances in genetic testing, and considers their implications for the diagnosis and treatment of FH.","PeriodicalId":55252,"journal":{"name":"Clinical Lipidology","volume":"13 1","pages":"379 - 385"},"PeriodicalIF":0.0,"publicationDate":"2015-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84457575","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}
G. Paradies, V. Paradies, F. M. Ruggiero, G. Petrosillo
Abstract Mitochondrial dysfunction is centrally involved in heart ischemia/reperfusion (I/R) injury. Increased reactive oxygen species production, impaired respiratory chain complexes activity and opening of the mitochondrial permeability transition pore have been suggested as possible factors responsible for mitochondrial dysfunction in heart I/R injury. Cardiolipin (CL), a phospholipid of the inner mitochondrial membrane, plays an important role in mitochondrial bioenergetics. CL alterations have been shown to play a causative role in mitochondrial dysfunction in a variety of pathological conditions, as well as in cell death. The role of CL alterations in mitochondrial dysfunction in heart I/R injury is here reviewed. Several cardioprotective strategies to prevent myocardial injury during I/R targeting mitochondrial CL are also examined.
{"title":"Cardiolipin alterations and mitochondrial dysfunction in heart ischemia/reperfusion injury","authors":"G. Paradies, V. Paradies, F. M. Ruggiero, G. Petrosillo","doi":"10.2217/clp.15.31","DOIUrl":"https://doi.org/10.2217/clp.15.31","url":null,"abstract":"Abstract Mitochondrial dysfunction is centrally involved in heart ischemia/reperfusion (I/R) injury. Increased reactive oxygen species production, impaired respiratory chain complexes activity and opening of the mitochondrial permeability transition pore have been suggested as possible factors responsible for mitochondrial dysfunction in heart I/R injury. Cardiolipin (CL), a phospholipid of the inner mitochondrial membrane, plays an important role in mitochondrial bioenergetics. CL alterations have been shown to play a causative role in mitochondrial dysfunction in a variety of pathological conditions, as well as in cell death. The role of CL alterations in mitochondrial dysfunction in heart I/R injury is here reviewed. Several cardioprotective strategies to prevent myocardial injury during I/R targeting mitochondrial CL are also examined.","PeriodicalId":55252,"journal":{"name":"Clinical Lipidology","volume":"13 1","pages":"415 - 429"},"PeriodicalIF":0.0,"publicationDate":"2015-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78752986","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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