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Article ; Online: Iron overload and programmed bone marrow cell death: Potential mechanistic insights.

Wudhikulprapan, Wanat / Chattipakorn, Siriporn C / Chattipakorn, Nipon / Kumfu, Sirinart

2024 Volume 754, Page(s) 109954

Abstract: Iron overload has detrimental effects on bone marrow mesenchymal stem cells (BMMSCs), cells crucial for bone marrow homeostasis and hematopoiesis support. Excessive iron accumulation leads to the production of reactive oxygen species (ROS), resulting in ... ...

Abstract	Iron overload has detrimental effects on bone marrow mesenchymal stem cells (BMMSCs), cells crucial for bone marrow homeostasis and hematopoiesis support. Excessive iron accumulation leads to the production of reactive oxygen species (ROS), resulting in cell death, cell cycle arrest, and disruption of vital cellular pathways. Although apoptosis has been extensively studied, other programmed cell death mechanisms including autophagy, necroptosis, and ferroptosis also play significant roles in iron overload-induced bone marrow cell death. Studies have highlighted the involvement of ROS production, DNA damage, MAPK pathways, and mitochondrial dysfunction in apoptosis. In addition, autophagy and ferroptosis are activated, as shown by the degradation of cellular components and lipid peroxidation, respectively. However, several compounds and antioxidants show promise in mitigating iron overload-induced cell death by modulating ROS levels, MAPK pathways, and mitochondrial integrity. Despite early indications, more comprehensive research and clinical studies are needed to better understand the interplay between these programmed cell death mechanisms and enable development of effective therapeutic strategies. This review article emphasizes the importance of studying multiple cell death pathways simultaneously and investigating potential rescuers to combat iron overload-induced bone marrow cell death.
MeSH term(s)	Humans ; Iron/metabolism ; Reactive Oxygen Species/metabolism ; Bone Marrow/metabolism ; Iron Overload/metabolism ; Apoptosis ; Bone Marrow Cells/metabolism
Chemical Substances	Iron (E1UOL152H7) ; Reactive Oxygen Species
Language	English
Publishing date	2024-03-01
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	523-x
ISSN	1096-0384 ; 0003-9861
ISSN (online)	1096-0384
ISSN	0003-9861
DOI	10.1016/j.abb.2024.109954
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Article ; Online: Correction: Kobroob et al. Effectiveness of N-Acetylcysteine in the Treatment of Renal Deterioration Caused by Long-Term Exposure to Bisphenol A.

Kobroob, Anongporn / Peerapanyasut, Wachirasek / Kumfu, Sirinart / Chattipakorn, Nipon / Wongmekiat, Orawan

Biomolecules

2023 Volume 13, Issue 12

Abstract: The authors would like to replace Figure 2 of the following published paper [ ... ]. ...

Abstract	The authors would like to replace Figure 2 of the following published paper [...].
Language	English
Publishing date	2023-12-12
Publishing country	Switzerland
Document type	Published Erratum
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom13121781
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Article ; Online: Iron overload cardiomyopathy: Using the latest evidence to inform future applications.

Kumfu, Sirinart / Chattipakorn, Siriporn C / Chattipakorn, Nipon

Experimental biology and medicine (Maywood, N.J.)

2022 Volume 247, Issue 7, Page(s) 574–583

Abstract: Iron overload can be the result of either dysregulated iron metabolism in the case of hereditary hemochromatosis or repeated blood transfusions in the case of secondary hemochromatosis (e.g. in β-thalassemia and sickle cell anemia patients). Under iron ... ...

Abstract	Iron overload can be the result of either dysregulated iron metabolism in the case of hereditary hemochromatosis or repeated blood transfusions in the case of secondary hemochromatosis (e.g. in β-thalassemia and sickle cell anemia patients). Under iron overload conditions, transferrin (Tf) saturation leads to an increase in non-Tf bound iron which can result in the generation of reactive oxygen species (ROS). These excess ROS can damage cellular components, resulting in the dysfunction of vital organs including iron overload cardiomyopathy (IOC). Multiple studies have demonstrated that L-type and T-type calcium channels are the main routes for iron uptake in the heart, and that calcium channel blockers, given either individually or in combination with standard iron chelators, confer cardioprotective effects under iron overload conditions. Treatment with antioxidants may also provide therapeutic benefits. Interestingly, recent studies have suggested that mitochondrial dynamics and regulated cell death (RCD) pathways are potential targets for pharmacological interventions against iron-induced cardiomyocyte injury. In this review, the potential therapeutic roles of iron chelators, antioxidants, iron uptake/metabolism modulators, mitochondrial dynamics modulators, and inhibitors of RCD pathways in IOC are summarized and discussed.
MeSH term(s)	Antioxidants/therapeutic use ; Cardiomyopathies/drug therapy ; Hemochromatosis/complications ; Hemochromatosis/drug therapy ; Hemochromatosis/metabolism ; Humans ; Iron/metabolism ; Iron Chelating Agents/metabolism ; Iron Chelating Agents/pharmacology ; Iron Chelating Agents/therapeutic use ; Iron Overload/complications ; Iron Overload/drug therapy ; Myocytes, Cardiac/metabolism ; Reactive Oxygen Species/metabolism
Chemical Substances	Antioxidants ; Iron Chelating Agents ; Reactive Oxygen Species ; Iron (E1UOL152H7)
Language	English
Publishing date	2022-02-07
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	4015-0
ISSN	1535-3699 ; 1525-1373 ; 0037-9727
ISSN (online)	1535-3699 ; 1525-1373
ISSN	0037-9727
DOI	10.1177/15353702221076397
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Article ; Online: Effects of Particulate Matter on Inflammation and Thrombosis: Past Evidence for Future Prevention.

Hantrakool, Sasinee / Kumfu, Sirinart / Chattipakorn, Siriporn C / Chattipakorn, Nipon

International journal of environmental research and public health

2022 Volume 19, Issue 14

Abstract: Ambient air pollution has become a common problem worldwide. Exposure to pollutant particles causes many health conditions, having a particular impact on pulmonary and cardiovascular disease. Increased understanding of the pathological processes related ... ...

Abstract	Ambient air pollution has become a common problem worldwide. Exposure to pollutant particles causes many health conditions, having a particular impact on pulmonary and cardiovascular disease. Increased understanding of the pathological processes related to these conditions may facilitate the prevention of the adverse impact of air pollution on our physical health. Evidence from in vitro, in vivo, and clinical studies has consistently shown that exposure to particulate matter could induce the inflammatory responses such as IL-6, TNF-α, IL-1β, as well as enhancing the oxidative stress. These result in vascular injury, adhesion molecule release, platelet activation, and thrombin generation, ultimately leading to a prothrombotic state. In this review, evidence on the effects of particulate matter on inflammation, oxidative stress, adhesion molecules, and coagulation pathways in enhancing the risk of thrombosis is comprehensively summarized and discussed. The currently available outcomes of interventional studies at a cellular level and clinical reports are also presented and discussed.
MeSH term(s)	Air Pollutants/analysis ; Air Pollutants/toxicity ; Air Pollution/adverse effects ; Air Pollution/analysis ; Humans ; Inflammation/chemically induced ; Oxidative Stress ; Particulate Matter/toxicity ; Thrombosis/etiology ; Thrombosis/prevention & control
Chemical Substances	Air Pollutants ; Particulate Matter
Language	English
Publishing date	2022-07-19
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2175195-X
ISSN	1660-4601 ; 1661-7827
ISSN (online)	1660-4601
ISSN	1661-7827
DOI	10.3390/ijerph19148771
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Article ; Online: The regulatory effects of PTPN6 on inflammatory process: Reports from mice to men.

Kiratikanon, Salin / Chattipakorn, Siriporn C / Chattipakorn, Nipon / Kumfu, Sirinart

Archives of biochemistry and biophysics

2022 Volume 721, Page(s) 109189

Abstract: Protein tyrosine phosphatase non-receptor type 6 (PTPN6) is a key regulatory protein in cellular signal transduction in the control of inflammation and cell death. Impairment of PTPN6 is known to be associated with human inflammatory diseases including ... ...

Abstract	Protein tyrosine phosphatase non-receptor type 6 (PTPN6) is a key regulatory protein in cellular signal transduction in the control of inflammation and cell death. Impairment of PTPN6 is known to be associated with human inflammatory diseases including neutrophilic dermatosis; however, comprehensive studies of PTPN6-associated neutrophilic dermatosis have not clearly identified the relationships involved. Reports from in vitro and in vivo studies revealed that inflammatory cytokines have increased in the white blood cells from PTPN6-knocked out mice, and systemic inflammation was also increased in these mice, resulting in skin inflammation in this model. Reports of PTPN6 regulatory functions through five pathophysiological mechanisms are summarized and discussed here including inhibition of myeloid differentiation primary response 88, enhancement of the regulatory function of receptor-interacting protein kinase, inhibition of receptor-interacting serine/threonine-protein kinase 3/mixed lineage kinase domain-like protein-dependent necroptosis, inhibition of caspase-8-dependent apoptosis, and inhibition of p38/mitogen-activated protein kinase. Treatments by blocking the pathways involved in signal transduction and inflammatory cytokine release are also summarized. Understanding this underlying mechanism could improve therapeutic strategies for neutrophilic dermatosis.
MeSH term(s)	Animals ; Humans ; Inflammation/metabolism ; Mice ; Protein Tyrosine Phosphatase, Non-Receptor Type 6/metabolism ; Signal Transduction ; Skin Diseases
Chemical Substances	PTPN6 protein, human (EC 3.1.3.48) ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 (EC 3.1.3.48)
Language	English
Publishing date	2022-03-17
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	523-x
ISSN	1096-0384 ; 0003-9861
ISSN (online)	1096-0384
ISSN	0003-9861
DOI	10.1016/j.abb.2022.109189
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Article ; Online: Withdrawn: Oxidative Stress and Inflammatory Markers of Cordocentesis Blood in Response to Fetal Anemia

Tongprasert, Fuanglada / Kumfu, Sirinart / Chattipakorn, Nipon / Tongsong, Theera

Current molecular medicine

2021

Language	English
Publishing date	2021-02-04
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2064873-X
ISSN	1875-5666 ; 1566-5240
ISSN (online)	1875-5666
ISSN	1566-5240
DOI	10.2174/1573405617666210204211744
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Article: Comparisons of serum non-transferrin-bound iron levels and fetal cardiac function between fetuses affected with hemoglobin Bart's disease and normal fetuses.

Jatavan, Phudit / Sekararithi, Rattanaporn / Jaiwongkam, Thidarat / Kumfu, Sirinart / Chattipakorn, Nipon / Tongsong, Theera

Frontiers in medicine

2023 Volume 9, Page(s) 1015306

Abstract: Objective: To compare the levels of Non-transferrin bound iron (NTBI) in fetuses with anemia, using Hb Bart's disease as a study model, and those in unaffected fetuses and to determine the association between fetal cardiac function and the levels of ... ...

Abstract	Objective: To compare the levels of Non-transferrin bound iron (NTBI) in fetuses with anemia, using Hb Bart's disease as a study model, and those in unaffected fetuses and to determine the association between fetal cardiac function and the levels of NTBI. Patients and methods: A prospective study was conducted on pregnancies at risk of fetal Hb Bart's disease. All fetuses underwent standard ultrasound examination at 18-22 weeks of gestation for fetal biometry, anomaly screening and fetal cardiac function. After that, 2 ml of fetal blood was taken by cordocentesis to measure NTBI by Labile Plasma Iron (LPI), serum iron, hemoglobin and hematocrit. The NTBI levels of both groups were compared and the correlation between NTBI and fetal cardiac function was determined. Results: A total of 50 fetuses, including 20 fetuses with Hb Bart's disease and 30 unaffected fetuses were recruited. There was a significant increase in the level of serum iron in the affected group (median: 22.7 vs. 9.7; Conclusion: Anemia caused by fetal Hb Bart's disease in pre-hydropic stage is significantly associated with fetal cardiac dysfunction and increased fetal serum NTBI levels which are significantly correlated with worsening cardiac dysfunction. Nevertheless, based on the limitations of the present study, further studies including long-term data are required to support a role of fetal anemia as well as increased fetal serum NTBI levels in development of subsequent heart failure or cardiac compromise among the survivors, possibly predisposing to cardiovascular disease in adult life.
Language	English
Publishing date	2023-01-03
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2775999-4
ISSN	2296-858X
ISSN	2296-858X
DOI	10.3389/fmed.2022.1015306
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Article: The regulatory effects of PTPN6 on inflammatory process: Reports from mice to men

Kiratikanon, Salin / Chattipakorn, Siriporn C. / Chattipakorn, Nipon / Kumfu, Sirinart

Archives of biochemistry and biophysics. 2022 May 30, v. 721

2022

Abstract	Protein tyrosine phosphatase non-receptor type 6 (PTPN6) is a key regulatory protein in cellular signal transduction in the control of inflammation and cell death. Impairment of PTPN6 is known to be associated with human inflammatory diseases including neutrophilic dermatosis; however, comprehensive studies of PTPN6-associated neutrophilic dermatosis have not clearly identified the relationships involved. Reports from in vitro and in vivo studies revealed that inflammatory cytokines have increased in the white blood cells from PTPN6-knocked out mice, and systemic inflammation was also increased in these mice, resulting in skin inflammation in this model. Reports of PTPN6 regulatory functions through five pathophysiological mechanisms are summarized and discussed here including inhibition of myeloid differentiation primary response 88, enhancement of the regulatory function of receptor-interacting protein kinase, inhibition of receptor-interacting serine/threonine-protein kinase 3/mixed lineage kinase domain-like protein-dependent necroptosis, inhibition of caspase-8-dependent apoptosis, and inhibition of p38/mitogen-activated protein kinase. Treatments by blocking the pathways involved in signal transduction and inflammatory cytokine release are also summarized. Understanding this underlying mechanism could improve therapeutic strategies for neutrophilic dermatosis.
Keywords	apoptosis ; biophysics ; cytokines ; humans ; inflammation ; models ; necroptosis ; protein-tyrosine-phosphatase ; regulatory proteins ; signal transduction ; skin diseases ; therapeutics
Language	English
Dates of publication	2022-0530
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	523-x
ISSN	1096-0384 ; 0003-9861
ISSN (online)	1096-0384
ISSN	0003-9861
DOI	10.1016/j.abb.2022.109189
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Article: Effects of air pollution on telomere length: Evidence from in vitro to clinical studies

Assavanopakun, Pheerasak / Sapbamrer, Ratana / Kumfu, Sirinart / Chattipakorn, Nipon / Chattipakorn, Siriporn C.

Environmental pollution. 2022 Nov. 01, v. 312

2022

Abstract: Air pollution remains the major environmental problem globally. There is extensive evidence showing that the variety of air pollutants from environmental and occupational exposures cause adverse effects to our health. The clinical symptoms of those ... ...

Abstract	Air pollution remains the major environmental problem globally. There is extensive evidence showing that the variety of air pollutants from environmental and occupational exposures cause adverse effects to our health. The clinical symptoms of those effects may present at a late stage, so surveillance is difficult to manage. Several biomarkers have been used for the early detection of health issues following exposure to air pollution, including the use of telomere length which indicates cellular senescence in response to oxidative stress. Oxidative stress is one of the most plausible mechanisms associated with exposure to air pollutants. Some specific contexts including age groups, gender, ethnicity, occupations, and health conditions, showed significant alterations in telomere length after exposure to air pollutants. Several reports demonstrated both negative and positive associations between telomere length and air pollution, the studies using different concentrations and exposure times to air pollution on the study of telomere lengths. Surprisingly, some studies reported that low levels of exposure to air pollutants (lower than regulated levels) caused the alterations in telomere length. Those findings suggest that telomere length could be one of most practical biomarkers in air pollution surveillance. Therefore, this review aimed to summarize and discuss the relationship between telomere length and exposure to air pollution. The knowledge from this review will be beneficial for the planning of public health to reduce health problems in the general population, particularly in vulnerable people, who still live in areas with high air pollution.
Keywords	air ; air pollution ; biomarkers ; cell senescence ; gender ; monitoring ; nationalities and ethnic groups ; oxidative stress ; public health ; telomeres
Language	English
Dates of publication	2022-1101
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	280652-6
ISSN	1873-6424 ; 0013-9327 ; 0269-7491
ISSN (online)	1873-6424
ISSN	0013-9327 ; 0269-7491
DOI	10.1016/j.envpol.2022.120096
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Article ; Online: Fetal Cardiac Cellular Damage Caused by Anemia in Utero in Hb Bart's Disease.

Jatavan, Phudit / Kumfu, Sirinart / Tongsong, Theera / Chattipakorn, Nipon

Current molecular medicine

2020 Volume 21, Issue 2, Page(s) 165–175

Abstract: Background: Severe fetal anemias can cause high output cardiac failure. Mitochondria are key regulators of cardiac function. However, the effects of an early phase of fetal anemia on the fetal heart and cardiac mitochondrial function are not known.: ... ...

Abstract	Background: Severe fetal anemias can cause high output cardiac failure. Mitochondria are key regulators of cardiac function. However, the effects of an early phase of fetal anemia on the fetal heart and cardiac mitochondrial function are not known. Objective: The aim of this study is to compare mitochondrial function and cardiac biochemical alterations in the fetal cardiac tissue between anemic and non-anemic fetuses. Materials and methods: A cross-sectional study was conducted in Fetuses affected by Hb Bart's disease (n=18) and non-anemic fetuses (n=10) at 17-20 weeks. Echocardiograms had been carried out in all cases to assess prenatal cardiac function. Cardiac tissues were collected after pregnancy termination for the determination of cardiac iron accumulation, mitochondrial function, including mitochondrial ROS production, mitochondrial depolarization and mitochondrial swelling, mitochondrial dynamics, inflammation, and apoptosis. Results: Prenatal cardiac function evaluated by ultrasound was comparable between the Hb Bart's and non-anemic groups. In Bart's group, the levels of cardiac mitochondrial depolarization and swelling, and the TNF-α level were significantly higher, compared to the non-anemic group. On the contrary, anti-inflammatory (IL-10) levels were significantly lower in the Hb Bart's group. Additionally, active caspase-3 and Bcl-2 expression were also significantly higher (P= 0.001, P=0.035) in Bart's group. The mitochondrial fission protein expression, including p-DRP1/total DRP1, was significantly higher in Bart's group. However, there was no difference in cardiac iron accumulation levels between these two groups. Conclusion: Despite equivalent prenatal cardiac function and comparable cardiac iron accumulation in the Bart's and non-anemic groups, fetal anemia is significantly associated with cardiac mitochondrial dysfunction, increased mitochondrial fission, and increased inflammation and apoptosis. These findings indicate that an early phase of fetal anemia without cardiac iron overload can lead to cardiac mitochondrial dysfunction in fetuses with Hb Bart's.
MeSH term(s)	Anemia/complications ; Anemia/diagnostic imaging ; Anemia/pathology ; Apoptosis ; Case-Control Studies ; Cross-Sectional Studies ; Female ; Fetal Diseases/diagnostic imaging ; Fetal Diseases/etiology ; Fetal Diseases/pathology ; Fetal Heart/diagnostic imaging ; Fetal Heart/metabolism ; Fetal Heart/pathology ; Heart Failure/diagnostic imaging ; Heart Failure/etiology ; Heart Failure/pathology ; Hemoglobins, Abnormal/analysis ; Hemoglobins, Abnormal/metabolism ; Humans ; Inflammation Mediators/metabolism ; Iron/metabolism ; Mitochondria, Heart/metabolism ; Mitochondria, Heart/pathology ; Oxidative Stress ; Pregnancy ; Ultrasonography, Prenatal
Chemical Substances	Hemoglobins, Abnormal ; Inflammation Mediators ; hemoglobin Bart's (9056-09-1) ; Iron (E1UOL152H7)
Language	English
Publishing date	2020-06-26
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2064873-X
ISSN	1875-5666 ; 1566-5240
ISSN (online)	1875-5666
ISSN	1566-5240
DOI	10.2174/1566524020666200610163546
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