Translational issues for mitoprotective agents as adjunct to reperfusion therapy in patients with ST‐segment elevation myocardial infarction

Pre‐clinical studies have indicated that mitoprotective drugs may add cardioprotection beyond rapid revascularization, antiplatelet therapy and risk modification. We review the clinical efficacy of mitoprotective drugs that have progressed to clinical testing comprising cyclosporine A, KAI‐9803, MTP...

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Published inJournal of cellular and molecular medicine Vol. 24; no. 5; pp. 2717 - 2729
Main Authors Bøtker, Hans Erik, Cabrera‐Fuentes, Hector Alejandro, Ruiz‐Meana, Marisol, Heusch, Gerd, Ovize, Michel
Format Journal Article
LanguageEnglish
Published England John Wiley & Sons, Inc 01.03.2020
Wiley Open Access
John Wiley and Sons Inc
Subjects
Adenosine triphosphate
Aging
Angioplasty
Animals
Apoptosis
Clinical Trials as Topic
Coronary vessels
cyclosporine A
Cyclosporins
Diabetes mellitus
Drug development
Dyslipidemia
Heart attacks
Heart failure
Homeostasis
Humans
Immunomodulators
ischaemia
Kinases
Life Sciences
Membrane permeability
Mitochondria
Mitochondria, Heart - pathology
Mitochondrial permeability transition pore
Myocardial infarction
Myocardial Reperfusion
Oxidative stress
Permeability
Protective Agents - pharmacology
Protective Agents - therapeutic use
Proteins
Reperfusion
Review
Reviews
Rodents
ST Elevation Myocardial Infarction - drug therapy
ST Elevation Myocardial Infarction - physiopathology
Translational Medical Research
ischaemia
cyclosporine A
reperfusion
mitochondria
myocardial infarction
Online AccessGet full text
ISSN1582-1838
1582-4934
1582-4934
DOI10.1111/jcmm.14953

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Abstract Pre‐clinical studies have indicated that mitoprotective drugs may add cardioprotection beyond rapid revascularization, antiplatelet therapy and risk modification. We review the clinical efficacy of mitoprotective drugs that have progressed to clinical testing comprising cyclosporine A, KAI‐9803, MTP131 and TRO 40303. Whereas cyclosporine may reduce infarct size in patients undergoing primary angioplasty as evaluated by release of myocardial ischaemic biomarkers and infarct size imaging, the other drugs were not capable of demonstrating this effect in the clinical setting. The absent effect leaves the role of the mitochondrial permeability transition pore for reperfusion injury in humans unanswered and indicates that targeting one single mechanism to provide mitoprotection may not be efficient. Moreover, the lack of effect may relate to favourable outcome with current optimal therapy, but conditions such as age, sex, diabetes, dyslipidaemia and concurrent medications may also alter mitochondrial function. However, as long as the molecular structure of the pore remains unknown and specific inhibitors of its opening are lacking, the mitochondrial permeability transition pore remains a target for alleviation of reperfusion injury. Nevertheless, taking conditions such as ageing, sex, comorbidities and co‐medication into account may be of paramount importance during the design of pre‐clinical and clinical studies testing mitoprotective drugs.
AbstractList Pre‐clinical studies have indicated that mitoprotective drugs may add cardioprotection beyond rapid revascularization, antiplatelet therapy and risk modification. We review the clinical efficacy of mitoprotective drugs that have progressed to clinical testing comprising cyclosporine A, KAI‐9803, MTP131 and TRO 40303. Whereas cyclosporine may reduce infarct size in patients undergoing primary angioplasty as evaluated by release of myocardial ischaemic biomarkers and infarct size imaging, the other drugs were not capable of demonstrating this effect in the clinical setting. The absent effect leaves the role of the mitochondrial permeability transition pore for reperfusion injury in humans unanswered and indicates that targeting one single mechanism to provide mitoprotection may not be efficient. Moreover, the lack of effect may relate to favourable outcome with current optimal therapy, but conditions such as age, sex, diabetes, dyslipidaemia and concurrent medications may also alter mitochondrial function. However, as long as the molecular structure of the pore remains unknown and specific inhibitors of its opening are lacking, the mitochondrial permeability transition pore remains a target for alleviation of reperfusion injury. Nevertheless, taking conditions such as ageing, sex, comorbidities and co‐medication into account may be of paramount importance during the design of pre‐clinical and clinical studies testing mitoprotective drugs.
Pre-clinical studies have indicated that mitoprotective drugs may add cardioprotection beyond rapid revascularization, antiplatelet therapy and risk modification. We review the clinical efficacy of mitoprotective drugs that have progressed to clinical testing comprising cyclosporine A, KAI-9803, MTP131 and TRO 40303. Whereas cyclosporine may reduce infarct size in patients undergoing primary angioplasty as evaluated by release of myocardial ischaemic biomarkers and infarct size imaging, the other drugs were not capable of demonstrating this effect in the clinical setting. The absent effect leaves the role of the mitochondrial permeability transition pore for reperfusion injury in humans unanswered and indicates that targeting one single mechanism to provide mitoprotection may not be efficient. Moreover, the lack of effect may relate to favourable outcome with current optimal therapy, but conditions such as age, sex, diabetes, dyslipidaemia and concurrent medications may also alter mitochondrial function. However, as long as the molecular structure of the pore remains unknown and specific inhibitors of its opening are lacking, the mitochondrial permeability transition pore remains a target for alleviation of reperfusion injury. Nevertheless, taking conditions such as ageing, sex, comorbidities and co-medication into account may be of paramount importance during the design of pre-clinical and clinical studies testing mitoprotective drugs.Pre-clinical studies have indicated that mitoprotective drugs may add cardioprotection beyond rapid revascularization, antiplatelet therapy and risk modification. We review the clinical efficacy of mitoprotective drugs that have progressed to clinical testing comprising cyclosporine A, KAI-9803, MTP131 and TRO 40303. Whereas cyclosporine may reduce infarct size in patients undergoing primary angioplasty as evaluated by release of myocardial ischaemic biomarkers and infarct size imaging, the other drugs were not capable of demonstrating this effect in the clinical setting. The absent effect leaves the role of the mitochondrial permeability transition pore for reperfusion injury in humans unanswered and indicates that targeting one single mechanism to provide mitoprotection may not be efficient. Moreover, the lack of effect may relate to favourable outcome with current optimal therapy, but conditions such as age, sex, diabetes, dyslipidaemia and concurrent medications may also alter mitochondrial function. However, as long as the molecular structure of the pore remains unknown and specific inhibitors of its opening are lacking, the mitochondrial permeability transition pore remains a target for alleviation of reperfusion injury. Nevertheless, taking conditions such as ageing, sex, comorbidities and co-medication into account may be of paramount importance during the design of pre-clinical and clinical studies testing mitoprotective drugs.
Author Bøtker, Hans Erik
Heusch, Gerd
Ruiz‐Meana, Marisol
Ovize, Michel
Cabrera‐Fuentes, Hector Alejandro
AuthorAffiliation 5 Tecnologico de Monterrey Centro de Biotecnologia‐FEMSA Monterrey Mexico
10 CarMeN Laboratory Hôpital Louis Pradel Hospices Civils de Lyon Université de Lyon and Explorations Fonctionnelles Cardiovasculaires INSERM U1060 Lyon France
1 Department of Cardiology Aarhus University Hospital Aarhus N Denmark
7 Vall d'Hebron Institut de Recerca University Hospital Vall d'Hebron‐Universitat Autònoma Barcelona Spain
4 Institute of Biochemistry Medical School Justus‐Liebig University Giessen Germany
6 Institute of Fundamental Medicine and Biology Kazan (Volga Region) Federal University Kazan Russian Federation
3 National Heart Research Institute Singapore National Heart Centre Singapore Singapore
9 Institute for Pathophysiology West German Heart and Vascular Center University of Essen. Medical School Essen Germany
8 Centro de Investigación Biomédica en Red‐CV CIBER‐CV Spain
2 SingHealth Duke‐NUS Cardiovascular Sciences Academic Clinical Programme and Cardiovascular and Metabolic Disorders Program Duke‐N
AuthorAffiliation_xml – name: 1 Department of Cardiology Aarhus University Hospital Aarhus N Denmark
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– name: 7 Vall d'Hebron Institut de Recerca University Hospital Vall d'Hebron‐Universitat Autònoma Barcelona Spain
– name: 10 CarMeN Laboratory Hôpital Louis Pradel Hospices Civils de Lyon Université de Lyon and Explorations Fonctionnelles Cardiovasculaires INSERM U1060 Lyon France
– name: 9 Institute for Pathophysiology West German Heart and Vascular Center University of Essen. Medical School Essen Germany
– name: 2 SingHealth Duke‐NUS Cardiovascular Sciences Academic Clinical Programme and Cardiovascular and Metabolic Disorders Program Duke‐National University of Singapore Medical School Singapore Singapore
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/31967733$$D View this record in MEDLINE/PubMed
https://hal.science/hal-02901843$$DView record in HAL
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ContentType Journal Article
Copyright 2020 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.
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IsDoiOpenAccess true
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Issue 5
Keywords ischaemia
cyclosporine A
reperfusion
mitochondria
myocardial infarction
Language English
License Attribution
2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.
Distributed under a Creative Commons Attribution 4.0 International License: http://creativecommons.org/licenses/by/4.0
This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
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Notes Funding information
HEB is supported by the Novo Nordisk Foundation (grant numbers NNF14OC0013337 and NNF15OC0016674); HACF is supported by the Russian Government Program for competitive growth of Kazan Federal University, Kazan (Russian Federation), by the Singapore Heart Foundation (SHF/FG657P/2017) and by the von Behring‐Rӧntgen‐Foundation (Marburg, Germany). MRM is funded by ISCIII (PI19‐01196), CIBER‐CV, Fundació MTV3‐122/C/2015, SEC‐2016 and the European Regional Development Fundings (ERDF‐FEDER); and GH is supported by the German Research Foundation (SFB 1116 B8). This article is based on the work of COST Action EU‐CARDIOPROTECTION (CA16225) and supported by COST (European Cooperation in Science and Technology).
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OpenAccessLink https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fjcmm.14953
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Snippet Pre‐clinical studies have indicated that mitoprotective drugs may add cardioprotection beyond rapid revascularization, antiplatelet therapy and risk...
Pre-clinical studies have indicated that mitoprotective drugs may add cardioprotection beyond rapid revascularization, antiplatelet therapy and risk...
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StartPage 2717
SubjectTerms Adenosine triphosphate
Aging
Angioplasty
Animals
Apoptosis
Clinical Trials as Topic
Coronary vessels
cyclosporine A
Cyclosporins
Diabetes mellitus
Drug development
Dyslipidemia
Heart attacks
Heart failure
Homeostasis
Humans
Immunomodulators
ischaemia
Kinases
Life Sciences
Membrane permeability
Mitochondria
Mitochondria, Heart - pathology
Mitochondrial permeability transition pore
Myocardial infarction
Myocardial Reperfusion
Oxidative stress
Permeability
Protective Agents - pharmacology
Protective Agents - therapeutic use
Proteins
Reperfusion
Review
Reviews
Rodents
ST Elevation Myocardial Infarction - drug therapy
ST Elevation Myocardial Infarction - physiopathology
Translational Medical Research
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Title Translational issues for mitoprotective agents as adjunct to reperfusion therapy in patients with ST‐segment elevation myocardial infarction
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fjcmm.14953
https://www.ncbi.nlm.nih.gov/pubmed/31967733
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https://www.proquest.com/docview/2343498014
https://hal.science/hal-02901843
https://pubmed.ncbi.nlm.nih.gov/PMC7077531
Volume 24
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