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Gasdermin D-mediated pyroptosis in myocardial ischemia and reperfusion injury:Cumulative evidence for future cardioprotective strategies

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Acta Pharmaceutica Sinica B 2023年第1期13卷 29-53页

作者： Panat Yanpiset Chayodom Maneechote Sirawit Sriwichaiin Natthaphat Siri-Angkul siriporn C.chattipakorn Nipon chattipakorn Cardiac Electrophysiology Research and Training Center Faculty of MedicineChiang Mai UniversityChiang Mai 50200Thailand Cardiac Electrophysiology Unit Department of PhysiologyFaculty of MedicineChiang Mai UniversityChiang Mai 50200Thailand Center of Excellence in Cardiac Electrophysiology Research Chiang Mai UniversityChiang Mai 50200Thailand Department of Oral Biology and Diagnostic Sciences Faculty of DentistryChiang Mai UniversityChiang Mai 50200Thailand

Cardiomyocyte death is one of the major mechanisms contributing to the development of myocardial infarction(MI)and myocardial ischemia/reperfusion(MI/R)*** to the limited regenerative ability of cardiomyocytes,understanding the mechanisms of cardiomyocyte death is ***,one of the regulated programmed cell death pathways,has recently been shown to play important roles in MI and MI/R *** is activated by damage-associated molecular patterns(DAMPs)that are released from damaged myocardial cells and activate the formation of an apoptosisassociated speck-like protein containing a CARD(ASC)interacting with NACHT,LRR,and PYD domains-containing protein 3(NLRP3),resulting in caspase-1 cleavage which promotes the activation of Gasdermin D(GSDMD).This pathway is known as the canonical *** has also been shown to be activated in a non-canonical pathway during MI and MI/R injury via caspase-4/5/*** of GSDMD has been shown to provide cardioprotection against MI and MI/R *** the effects of MI or MI/R injury on pyroptosis have previously been discussed,knowledge concerning the roles of GSDMD in these settings remains *** this review,the evidence from in vitro,in vivo,and clinical studies focusing on cardiac GSDMD activation during MI and MI/R injury is comprehensively summarized and *** from this review will help pave the way for a new therapeutic target in ischemic heart disease.

关键词： Pyroptosis Gasdermin D Heart Ischemia Ischemia-reperfusion injury Myocardial infarction

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PPARγ activator,rosiglitazone:Is it beneficial or harmful to the cardiovascular system?

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World Journal of Cardiology 2011年第5期3卷 144-152页

作者： Siripong Palee siriporn chattipakorn Arintaya Phrommintikul Nipon chattipakorn Nipon chattipakorn Cardiac Electrophysiology UnitDepartment of PhysiologyFaculty of MedicineChiang Mai University Cardiac Electrophysiology Research and Training Center Faculty of MedicineChiang Mai University Faculty of Dentistry Chiang Mai University Department of Medicine Faculty of MedicineChiang Mai University

Rosiglitazone is a synthetic agonist of peroxisome proliferator-activated receptor γ which is used to improve insulin resistance in patients with type II diabetes. Rosiglitazone exerts its glucose-lowering effects by improving insulin sensitivity. Data from various studies in the past decade suggest that the therapeutic effects of rosiglitazone reach far beyond its use as an insulin sensitizer since it also has other benefits on the cardiovascular system such as improvement of contractile dysfunction, inhibition of the inflammatory response by reducing neutrophil and macrophage accumulation, and the protection of myocardial injury during ischemic/reperfusion in different animal models. Previous clinical studies in type II diabetes patients demonstrated that rosiglitazone played an important role in protecting against arteriosclerosis by normalizing the metabolic disorders and reducing chronic inflammation of the vascular system. Despite these benefits, inconsistent findings have been reported, and growing evidence has demonstrated adverse effects of rosiglitazone on the cardiovascular system, including increased risk of acute myocardial infarction, heart failure and chronic heart failure. As a result, rosiglitazone has been recently withdrawn from EU countries. Nevertheless, the effect of rosiglitazone on ischemic heart disease has not yet been firmly established. Future prospective clinical trials designed for the specific purpose of establishing the cardiovascular benefit or risk of rosiglitazone would be the best way to resolve the uncertainties regarding the safety of rosiglitazone in patients with heart disease.

关键词： Rosiglitazone Ischemic reperfusion injury Heart disease TypeⅡdiabetic Thiazolidinediones

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Calcium channels and iron uptake into the heart

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World Journal of Cardiology 2011年第7期3卷 215-218页

作者： Nipon chattipakorn Sirinart Kumfu Suthat Fucharoen siriporn chattipakorn Department of Physiology Cardiac Electrophysiology UnitFaculty of MedicineChiang Mai UniversityChiang Mai 50200Thailand Cardiac Electrophysiology Research and Training Center Faculty of MedicineChiang Mai UniversityChiang Mai 50200Thailand The Institute of Molecular Biosciences Mahidol UniversityBangkok 73170Thailand Faculty of Dentistry Chiang Mai UniversityChiang Mai 50200Thailand

Iron overload can lead to iron deposits in many tissues,particularly in the *** has also been shown to be associated with elevated oxidative stress in *** cardiac iron deposits can lead to iron overload cardiomyopathy,a condition which provokes mortality due to heart failure in iron-overloaded ***,the mechanism of iron uptake into cardiomyocytes is still not clearly *** evidence suggests L-type Ca2+channels(LTCCs)as a possible pathway for ferrous iron(Fe2+)uptake into cardiomyocytes under iron overload ***,controversy still exists since some findings on pharmacological interventions and those using different cell types do not support LTCC’s role as a portal for iron uptake in cardiac ***,T-type Ca2+channels (TTCC)have been shown to play an important role in the diseased *** TTCC and iron uptake in cardiomyocytes has not been investigated greatly,a recent finding indicated that TTCC could be an important portal in thalassemic *** this review,comprehensive findings collected from previous studies as well as a discussion of the controversy regarding iron uptake mechanisms into cardiomyocytes via calcium channels are presented with the hope that understanding the cellular iron uptake mechanism in cardiomyocytes will lead to improved treatment and prevention strategies,particularly in iron-overloaded patients.

关键词： Cardiomyocytes L-type calcium channel T-type calcium channels Iron overload Thalassemia

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Early detection of cardiac involvement in thalassemia: From bench to bedside perspective

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World Journal of Cardiology 2013年第8期5卷 270-279页

作者： Nut Koonrungsesomboon siriporn C chattipakorn Suthat Fucharoen Nipon chattipakorn Cardiac Electrophysiology Research and Training Center Department of Physiology Faculty of Medicine Chiang Mai University Department of Pharmacology Faculty of Medicine Chiang Mai University Department of Oral Biology and Diagnostic Science Faculty of Dentistry Chiang Mai University Thalassemia Research Center Institute of Molecular Medicine Mahidol University

Myocardial siderosis is known as the major cause of death in thalassemia major(TM) patients since it can lead to iron overload *** this condition can be prevented if timely effective intensive chelation is given to patients,the mortality rate of iron overload cardiomyopathy still remains high due to late detection of this *** direct and indirect methods of iron assessment,including serum ferritin level,echocardiogram,non-transferrin-bound iron,cardiac magnetic resonance T2*,heart rate variability,and liver biopsy and myocardial biopsy,have been proposed for early detection of cardiac iron overload in TM ***,controversial evidence and limitations of their use in clinical practice *** this review article,all of these iron assessment methods that have been proposed or used to directly or indirectly determine the cardiac iron status in TM reported from both basic and clinical studies are comprehensively summarized and *** there has been growing evidence in the past decades that cardiac magnetic resonance imaging as well as cardiac autonomic status known as the heart rate variability can provide early detection of cardiac involvement in TM patients,these two methods are also presented and *** existing controversy regarding the assessment of cardiac involvement in thalassemia is also discussed.

关键词： Thalassemia Iron overload Cardiomyopathy Serum ferritin Heart rate variability Magnetic resonance Non-transferrin-bound iron

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Phosphodiesterase-3 inhibitor （cilostazol） attenuates oxidative stress-induced mitochondrial dysfunction in the heart

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Journal of Geriatric Cardiology 2014年第2期11卷 151-157页

作者： siriporn C. Chattipakom Savitree Thummasorn Jantira Sanit Nipon chattipakorn Cardiac Electrophysiology Research and Training Center Department of Physiology Faculty of Medicine Chiang Mai University Chiang Mai 50200 Thailand Faculty of Dentistry Chiang Mai University Chiang Mai 50200 Thailand Biomedical Engineering Center Chiang Mai University Chiang Mai 50200 Thailand

Background Cilostazol is a type 3 phosphodiesterase inhibitor which has been previously demonstrated to prevent the occurrence of tachyarrhythmia and improve defibrillation efficacy. However, the mechanism for this beneficial effect is still unclear. Since cardiac mito-chondria have been shown to play a crucial role in fatal cardiac arrhythmias and that oxidative stress is one of the main contributors to arr-hythmia generation, we tested the effects of cilostazol on cardiac mitochondria under severe oxidative stress. Methods Mitochondria were isolated from rat hearts and treated with H2O2 to induce oxidative stress. Cilostazol, at various concentrations, was used to study its protective effects. Pharmacological interventions, including a mitochondrial permeability transition pore （mPTP） blocker, cyclosporine A （CsA）, and an inner membrane anion channel （IMAC） blocker, 4＇-chlorodiazepam （CDP）, were used to investigate the mechanistic role of cilostazol on cardiac mitochondria. Cardiac mitochondrial reactive oxygen species （ROS） production, mitochondrial membrane potential change and mi-tochondrial swelling were determined as indicators of cardiac mitochondrial function. Results Cilostazol preserved cardiac mitochondrial function when exposed to oxidative stress by preventing mitochondrial depolarization, mitochondrial swelling, and decreasing ROS produc-tion. Conclusions Our findings suggest that cardioprotective effects of cilostazol reported previously could be due to its prevention of car-diac mitochondrial dysfunction caused by severe oxidative stress.

关键词： Phosphodiesterase-3 inhibitor Cilostazol Mitochondria Heart Oxidative stress Membrane potential Ischemia

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