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Article ; Online: Hyperpolarization-activated cyclic nucleotide-gated channel inhibitor in myocardial infarction: Potential benefits beyond heart rate modulation.

Sripusanapan, Adivitch / Yanpiset, Panat / Sriwichaiin, Sirawit / Siri-Angkul, Natthaphat / Chattipakorn, Siriporn C / Chattipakorn, Nipon

Acta physiologica (Oxford, England)

2024 Volume 240, Issue 3, Page(s) e14085

Abstract: Myocardial infarction (MI) and its associated complications including ventricular arrhythmias and heart failure are responsible for a significant incidence of morbidity and mortality worldwide. The ensuing cardiomyocyte loss results in neurohormone- ... ...

Abstract	Myocardial infarction (MI) and its associated complications including ventricular arrhythmias and heart failure are responsible for a significant incidence of morbidity and mortality worldwide. The ensuing cardiomyocyte loss results in neurohormone-driven cardiac remodeling, which leads to chronic heart failure in MI survivors. Ivabradine is a heart rate modulation agent currently used in treatment of chronic heart failure with reduced ejection fraction. The canonical target of ivabradine is the hyperpolarization-activated cyclic nucleotide-gated channels (HCN) in cardiac pacemaker cells. However, in post-MI hearts, HCN can also be expressed ectopically in non-pacemaker cardiomyocytes. There is an accumulation of intriguing evidence to suggest that ivabradine also possesses cardioprotective effects that are independent of heart rate reduction. This review aims to summarize and discuss the reported cardioprotective mechanisms of ivabradine beyond heart rate modulation in myocardial infarction through various molecular mechanisms including the prevention of reactive oxygen species-induced mitochondrial damage, improvement of autophagy system, modulation of intracellular calcium cycling, modification of ventricular electrophysiology, and regulation of matrix metalloproteinases.
MeSH term(s)	Humans ; Ivabradine/pharmacology ; Ivabradine/therapeutic use ; Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels ; Heart Rate/physiology ; Benzazepines/pharmacology ; Myocardial Infarction/drug therapy ; Heart Failure/drug therapy ; Myocytes, Cardiac
Chemical Substances	Ivabradine (3H48L0LPZQ) ; Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels ; Benzazepines
Language	English
Publishing date	2024-01-17
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2218636-0
ISSN	1748-1716 ; 1748-1708
ISSN (online)	1748-1716
ISSN	1748-1708
DOI	10.1111/apha.14085
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Article ; Online: Fibroblast Growth Factor 23 and Osteoporosis: Evidence from Bench to Bedside.

Sirikul, Wachiranun / Siri-Angkul, Natthaphat / Chattipakorn, Nipon / Chattipakorn, Siriporn C

International journal of molecular sciences

2022 Volume 23, Issue 5

Abstract: Osteoporosis is a chronic debilitating disease caused by imbalanced bone remodeling processes that impair the structural integrity of bone. Over the last ten years, the association between fibroblast growth factor 23 (FGF23) and osteoporosis has been ... ...

Abstract	Osteoporosis is a chronic debilitating disease caused by imbalanced bone remodeling processes that impair the structural integrity of bone. Over the last ten years, the association between fibroblast growth factor 23 (FGF23) and osteoporosis has been studied in both pre-clinical and clinical investigations. FGF23 is a bone-derived endocrine factor that regulates mineral homeostasis via the fibroblast growth factor receptors (FGFRs)/αKlotho complex. These receptors are expressed in kidney and the parathyroid gland. Preclinical studies have supported the link between the local actions of FGF23 on the bone remodeling processes. In addition, clinical evidence regarding the effects of FGF23 on bone mass and fragility fractures suggest potential diagnostic and prognostic applications of FGF23 in clinical contexts, particularly in elderly and patients with chronic kidney disease. However, inconsistent findings exist and there are areas of uncertainty requiring exploration. This review comprehensively summarizes and discusses preclinical and clinical reports on the roles of FGF23 on osteoporosis, with an emphasis on the local action, as opposed to the systemic action, of FGF23 on the bone. Current gaps in knowledge and future research directions are also suggested to encourage further rigorous research in this important field.
MeSH term(s)	Aged ; Bone and Bones/metabolism ; Fibroblast Growth Factor-23 ; Fibroblast Growth Factors/metabolism ; Glucuronidase/genetics ; Humans ; Osteoporosis ; Receptors, Fibroblast Growth Factor/metabolism
Chemical Substances	Receptors, Fibroblast Growth Factor ; Fibroblast Growth Factors (62031-54-3) ; Fibroblast Growth Factor-23 (7Q7P4S7RRE) ; Glucuronidase (EC 3.2.1.31)
Language	English
Publishing date	2022-02-24
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23052500
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Article ; Online: The mechanistic insights of the arrhythmogenic effect of trastuzumab.

Siri-Angkul, Natthaphat / Chattipakorn, Siriporn C / Chattipakorn, Nipon

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2021 Volume 139, Page(s) 111620

Abstract: Cardiovascular diseases and cancers are the leading causes of deaths globally, and an increasing proportion of cancer patients is suffering from cardiac adverse effects of chemotherapeutic drugs. Trastuzumab, a monoclonal antibody that inhibits the ... ...

Abstract	Cardiovascular diseases and cancers are the leading causes of deaths globally, and an increasing proportion of cancer patients is suffering from cardiac adverse effects of chemotherapeutic drugs. Trastuzumab, a monoclonal antibody that inhibits the activity of the human epidermal growth factor receptor 2 (HER2), is a potent targeted therapy for HER2-positive malignancies. Despite the impressive antineoplastic efficacy, the cardiotoxicity of trastuzumab frequently limits its use. Trastuzumab-induced cardiac contractile dysfunction has been extensively studied, yet the electrophysiological side effect of trastuzumab remains poorly characterized. Growing evidence from basic and clinical studies supports the link between trastuzumab treatment and arrhythmias. This review comprehensively summarizes relevant information from those reports, discusses their limitations, and suggests future research directions. We aim to encourage further investigations that will provide valuable insights to devise cardioprotective strategies against trastuzumab-induced cardiotoxicity.
MeSH term(s)	Animals ; Antineoplastic Agents/adverse effects ; Arrhythmias, Cardiac/chemically induced ; Cardiotoxicity/drug therapy ; Humans ; Myocardial Contraction/drug effects ; Receptor, ErbB-2/genetics ; Trastuzumab/adverse effects
Chemical Substances	Antineoplastic Agents ; ERBB2 protein, human (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1) ; Trastuzumab (P188ANX8CK)
Language	English
Publishing date	2021-04-23
Publishing country	France
Document type	Journal Article ; Review
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/j.biopha.2021.111620
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Article ; Online: Corrigendum to "Acetylcholinesterase inhibitor ameliorates doxorubicin-induced cardiotoxicity through reducing RIP1-mediated necroptosis" [Pharmacol. Res. 173 (2021) 105882].

Khuanjing, Thawatchai / Ongnok, Benjamin / Maneechote, Chayodom / Siri-Angkul, Natthaphat / Prathumsap, Nanthip / Arinno, Apiwan / Chunchai, Titikorn / Arunsak, Busarin / Chattipakorn, Siriporn C / Chattipakorn, Nipon

Pharmacological research

2024 Volume 203, Page(s) 107147

Language	English
Publishing date	2024-04-01
Publishing country	Netherlands
Document type	Published Erratum
ZDB-ID	1003347-6
ISSN	1096-1186 ; 0031-6989 ; 1043-6618
ISSN (online)	1096-1186
ISSN	0031-6989 ; 1043-6618
DOI	10.1016/j.phrs.2024.107147
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Article ; Online: Fibroblast Growth Factor 23 and Osteoporosis

Wachiranun Sirikul / Natthaphat Siri-Angkul / Nipon Chattipakorn / Siriporn C. Chattipakorn

International Journal of Molecular Sciences, Vol 23, Iss 2500, p

Evidence from Bench to Bedside

2022 Volume 2500

Abstract	Osteoporosis is a chronic debilitating disease caused by imbalanced bone remodeling processes that impair the structural integrity of bone. Over the last ten years, the association between fibroblast growth factor 23 (FGF23) and osteoporosis has been studied in both pre-clinical and clinical investigations. FGF23 is a bone-derived endocrine factor that regulates mineral homeostasis via the fibroblast growth factor receptors (FGFRs)/αKlotho complex. These receptors are expressed in kidney and the parathyroid gland. Preclinical studies have supported the link between the local actions of FGF23 on the bone remodeling processes. In addition, clinical evidence regarding the effects of FGF23 on bone mass and fragility fractures suggest potential diagnostic and prognostic applications of FGF23 in clinical contexts, particularly in elderly and patients with chronic kidney disease. However, inconsistent findings exist and there are areas of uncertainty requiring exploration. This review comprehensively summarizes and discusses preclinical and clinical reports on the roles of FGF23 on osteoporosis, with an emphasis on the local action, as opposed to the systemic action, of FGF23 on the bone. Current gaps in knowledge and future research directions are also suggested to encourage further rigorous research in this important field.
Keywords	FGF23 ; osteoblast ; osteoclast ; biochemical markers ; bone remodeling ; osteoporosis ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	306 ; 616
Language	English
Publishing date	2022-02-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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

Yanpiset, Panat / Maneechote, Chayodom / Sriwichaiin, Sirawit / Siri-Angkul, Natthaphat / Chattipakorn, Siriporn C / Chattipakorn, Nipon

Acta pharmaceutica Sinica. B

2022 Volume 13, Issue 1, Page(s) 29–53

Abstract: Cardiomyocyte death is one of the major mechanisms contributing to the development of myocardial infarction (MI) and myocardial ischemia/reperfusion (MI/R) injury. Due to the limited regenerative ability of cardiomyocytes, understanding the mechanisms of ...

Abstract	Cardiomyocyte death is one of the major mechanisms contributing to the development of myocardial infarction (MI) and myocardial ischemia/reperfusion (MI/R) injury. Due to the limited regenerative ability of cardiomyocytes, understanding the mechanisms of cardiomyocyte death is necessary. Pyroptosis, one of the regulated programmed cell death pathways, has recently been shown to play important roles in MI and MI/R injury. Pyroptosis is activated by damage-associated molecular patterns (DAMPs) that are released from damaged myocardial cells and activate the formation of an apoptosis-associated 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 pathway. GSDMD has also been shown to be activated in a non-canonical pathway during MI and MI/R injury
Language	English
Publishing date	2022-08-13
Publishing country	Netherlands
Document type	Journal Article ; Review
ISSN	2211-3835
ISSN	2211-3835
DOI	10.1016/j.apsb.2022.08.007
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Article ; Online: Angiotensin converting enzyme 2 at the interface between renin-angiotensin system inhibition and coronavirus disease 2019.

Siri-Angkul, Natthaphat / Chattipakorn, Siriporn C / Chattipakorn, Nipon

The Journal of physiology

2020 Volume 598, Issue 19, Page(s) 4181–4195

Abstract: The coronavirus disease 2019 (COVID-19) is the third major coronavirus outbreak of this century. Its aetiological agent, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), requires angiotensin converting enzyme 2 (ACE2) for cellular entry. ...

Abstract	The coronavirus disease 2019 (COVID-19) is the third major coronavirus outbreak of this century. Its aetiological agent, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), requires angiotensin converting enzyme 2 (ACE2) for cellular entry. The commonly used angiotensin converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) could affect SARS-CoV-2 infectivity and may alter COVID-19 disease progression by altering ACE2 expression. Current evidence of ACEI/ARB-ACE2 interaction as well as the effects of ACEIs/ARBs on viral-associated acute lung injury is summarized and discussed in this review. This review assesses the evidence gathered so far and highlights the research that needs to be done to help inform clinical decision making.
MeSH term(s)	Angiotensin Receptor Antagonists/pharmacology ; Angiotensin Receptor Antagonists/therapeutic use ; Angiotensin-Converting Enzyme 2/metabolism ; Angiotensin-Converting Enzyme Inhibitors/pharmacology ; Angiotensin-Converting Enzyme Inhibitors/therapeutic use ; Animals ; COVID-19/drug therapy ; COVID-19/metabolism ; Humans ; Renin-Angiotensin System/drug effects
Chemical Substances	Angiotensin Receptor Antagonists ; Angiotensin-Converting Enzyme Inhibitors ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
Keywords	covid19
Language	English
Publishing date	2020-08-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/JP280138
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Article ; Online: Silencing of lipocalin-2 improves cardiomyocyte viability under iron overload conditions via decreasing mitochondrial dysfunction and apoptosis.

Kumfu, Sirinart / Siri-Angkul, Natthaphat / Chattipakorn, Siriporn C / Chattipakorn, Nipon

Journal of cellular physiology

2020 Volume 236, Issue 7, Page(s) 5108–5120

Abstract: This study aimed to investigate the mechanistic roles of LCN-2 and LCN-2 receptors (LCN-2R) as iron transporters in cardiomyocytes under iron overload condition. H9c2 cardiomyocytes were treated with either LCN-2 small interfering RNA (siRNA) or LCN-2R ... ...

Abstract	This study aimed to investigate the mechanistic roles of LCN-2 and LCN-2 receptors (LCN-2R) as iron transporters in cardiomyocytes under iron overload condition. H9c2 cardiomyocytes were treated with either LCN-2 small interfering RNA (siRNA) or LCN-2R siRNA or L-type or T-type calcium channel (LTCC or TTCC) blockers, or iron chelator deferiprone (DFP). After the treatments, the cells were exposed to Fe
MeSH term(s)	Animals ; Apoptosis/physiology ; Calcium Channels, L-Type/metabolism ; Calcium Channels, T-Type/metabolism ; Cell Line ; Cell Survival/genetics ; Deferiprone/pharmacology ; Iron/metabolism ; Iron Overload/pathology ; Lipocalin-2/genetics ; Mitochondria/pathology ; Myocytes, Cardiac/metabolism ; RNA Interference ; RNA, Small Interfering/genetics ; Rats
Chemical Substances	Calcium Channels, L-Type ; Calcium Channels, T-Type ; Lcn2 protein, rat ; Lipocalin-2 ; RNA, Small Interfering ; Deferiprone (2BTY8KH53L) ; Iron (E1UOL152H7)
Language	English
Publishing date	2020-12-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3116-1
ISSN	1097-4652 ; 0021-9541
ISSN (online)	1097-4652
ISSN	0021-9541
DOI	10.1002/jcp.30219
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Article ; Online: Targeting necroptosis as therapeutic potential in chronic myocardial infarction.

Piamsiri, Chanon / Maneechote, Chayodom / Siri-Angkul, Natthaphat / Chattipakorn, Siriporn C / Chattipakorn, Nipon

Journal of biomedical science

2021 Volume 28, Issue 1, Page(s) 25

Abstract: Cardiovascular diseases (CVDs) are considered the predominant cause of morbidity and mortality globally. Of these, myocardial infarction (MI) is the most common cause of CVD mortality. MI is a life-threatening condition which occurs when coronary ... ...

Abstract	Cardiovascular diseases (CVDs) are considered the predominant cause of morbidity and mortality globally. Of these, myocardial infarction (MI) is the most common cause of CVD mortality. MI is a life-threatening condition which occurs when coronary perfusion is interrupted leading to cardiomyocyte death. Subsequent to MI, consequences include adverse cardiac remodeling and cardiac dysfunction mainly contribute to the development of heart failure (HF). It has been shown that loss of functional cardiomyocytes in MI-induced HF are associated with several cell death pathways, in particular necroptosis. Although the entire mechanism underlying necroptosis in MI progression is still not widely recognized, some recent studies have reported beneficial effects of necroptosis inhibitors on cell viability and cardiac function in chronic MI models. Therefore, extensive investigation into the necroptosis signaling pathway is indicated for further study. This article comprehensively reviews the context of the underlying mechanisms of necroptosis in chronic MI-induced HF in in vitro, in vivo and clinical studies. These findings could inform ways of developing novel therapeutic strategies to improve the clinical outcomes in MI patients from this point forward.
MeSH term(s)	Animals ; Chronic Disease/therapy ; Heart Failure/therapy ; Humans ; Mice ; Myocardial Infarction/therapy ; Necroptosis
Language	English
Publishing date	2021-04-09
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1193378-1
ISSN	1423-0127 ; 1021-7770
ISSN (online)	1423-0127
ISSN	1021-7770
DOI	10.1186/s12929-021-00722-w
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Article ; Online: Mitochondrial dysfunction in fatal ventricular arrhythmias.

Wongtanasarasin, Wachira / Siri-Angkul, Natthaphat / Wittayachamnankul, Borwon / Chattipakorn, Siriporn C / Chattipakorn, Nipon

Acta physiologica (Oxford, England)

2021 Volume 231, Issue 4, Page(s) e13624

Abstract: Ventricular fibrillation (VF) and sudden cardiac arrest (SCA) remain some of the most important public health concerns worldwide. For the past 50 years, the recommendation in the Advanced Cardiac Life Support (ACLS) guidelines has been that ... ...

Abstract	Ventricular fibrillation (VF) and sudden cardiac arrest (SCA) remain some of the most important public health concerns worldwide. For the past 50 years, the recommendation in the Advanced Cardiac Life Support (ACLS) guidelines has been that defibrillation is the only option for shockable cardiac arrest. There is growing evidence to demonstrate that mitochondria play a vital role in the outcome of postresuscitation cardiac function. Although targeting mitochondria to improve resuscitation outcome following cardiac arrest has been proposed for many years, understanding concerning the changes in mitochondria during cardiac arrest, especially in the case of VF, is still limited. In addition, despite new research initiatives and improved medical technology, the overall survival rates of patients with SCA still remain the same. Understanding cardiac mitochondrial alterations during fatal arrhythmias may help to enable the formulation of strategies to improve the outcomes of resuscitation. The attenuation of cardiac mitochondrial dysfunction during VF through pharmacological intervention as well as ischaemic postconditioning could also be a promising target for intervention and inform a new paradigm of treatments. In this review, the existing evidence available from in vitro, ex vivo and in vivo studies regarding the roles of mitochondrial dysfunction during VF is comprehensively summarized and discussed. In addition, the effects of interventions targeting cardiac mitochondria during fatal ventricular arrhythmias are presented. Since there are no clinical reports from studies targeting mitochondria to improve resuscitation outcome available, this review will provide important information to encourage further investigations in a clinical setting.
MeSH term(s)	Cardiopulmonary Resuscitation ; Heart ; Heart Arrest ; Humans ; Mitochondria, Heart ; Ventricular Fibrillation/therapy
Language	English
Publishing date	2021-02-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2218636-0
ISSN	1748-1716 ; 1748-1708
ISSN (online)	1748-1716
ISSN	1748-1708
DOI	10.1111/apha.13624
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