A Mitochondrial Basis for Heart Failure Progression
(2024) In Cardiovascular Drugs and Therapy- Abstract
In health, the human heart is able to match ATP supply and demand perfectly. It requires 6 kg of ATP per day to satisfy demands of external work (mechanical force generation) and internal work (ion movements and basal metabolism). The heart is able to link supply with demand via direct responses to ADP and AMP concentrations but calcium concentrations within myocytes play a key role, signalling both inotropy, chronotropy and matched increases in ATP production. Calcium/calmodulin-dependent protein kinase (CaMKII) is a key adapter to increased workload, facilitating a greater and more rapid calcium concentration change. In the failing heart, this is dysfunctional and ATP supply is impaired. This review aims to examine the mechanisms and... (More)
In health, the human heart is able to match ATP supply and demand perfectly. It requires 6 kg of ATP per day to satisfy demands of external work (mechanical force generation) and internal work (ion movements and basal metabolism). The heart is able to link supply with demand via direct responses to ADP and AMP concentrations but calcium concentrations within myocytes play a key role, signalling both inotropy, chronotropy and matched increases in ATP production. Calcium/calmodulin-dependent protein kinase (CaMKII) is a key adapter to increased workload, facilitating a greater and more rapid calcium concentration change. In the failing heart, this is dysfunctional and ATP supply is impaired. This review aims to examine the mechanisms and pathologies that link increased energy demand to this disrupted situation. We examine the roles of calcium loading, oxidative stress, mitochondrial structural abnormalities and damage-associated molecular patterns.
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- author
- Watson, William D. ; Arvidsson, Per M. LU ; Miller, Jack J.J. ; Lewis, Andrew J. and Rider, Oliver J.
- organization
- publishing date
- 2024
- type
- Contribution to journal
- publication status
- in press
- subject
- keywords
- ATP, Calcium, Heart failure, Mitochondria, Redox
- in
- Cardiovascular Drugs and Therapy
- publisher
- Springer
- external identifiers
-
- scopus:85196106234
- ISSN
- 0920-3206
- DOI
- 10.1007/s10557-024-07582-0
- language
- English
- LU publication?
- yes
- id
- 203e5ff2-8c2e-4dcf-aec1-df2141860625
- date added to LUP
- 2024-09-11 15:28:09
- date last changed
- 2024-09-11 15:28:24
@article{203e5ff2-8c2e-4dcf-aec1-df2141860625,
abstract = {{<p>In health, the human heart is able to match ATP supply and demand perfectly. It requires 6 kg of ATP per day to satisfy demands of external work (mechanical force generation) and internal work (ion movements and basal metabolism). The heart is able to link supply with demand via direct responses to ADP and AMP concentrations but calcium concentrations within myocytes play a key role, signalling both inotropy, chronotropy and matched increases in ATP production. Calcium/calmodulin-dependent protein kinase (CaMKII) is a key adapter to increased workload, facilitating a greater and more rapid calcium concentration change. In the failing heart, this is dysfunctional and ATP supply is impaired. This review aims to examine the mechanisms and pathologies that link increased energy demand to this disrupted situation. We examine the roles of calcium loading, oxidative stress, mitochondrial structural abnormalities and damage-associated molecular patterns.</p>}},
author = {{Watson, William D. and Arvidsson, Per M. and Miller, Jack J.J. and Lewis, Andrew J. and Rider, Oliver J.}},
issn = {{0920-3206}},
keywords = {{ATP; Calcium; Heart failure; Mitochondria; Redox}},
language = {{eng}},
publisher = {{Springer}},
series = {{Cardiovascular Drugs and Therapy}},
title = {{A Mitochondrial Basis for Heart Failure Progression}},
url = {{http://dx.doi.org/10.1007/s10557-024-07582-0}},
doi = {{10.1007/s10557-024-07582-0}},
year = {{2024}},
}