Mitochondrial Reactive Oxygen Species Dysregulation in Heart Failure with Preserved Ejection Fraction: A Fraction of the Whole
Fraction (chemistry)
DOI:
10.20944/preprints202409.2167.v1
Publication Date:
2024-09-30T02:53:29Z
AUTHORS (3)
ABSTRACT
Heart failure with preserved ejection fraction (HFpEF) is a multifariousness syndrome, account-ing for over half of heart (HF) patients receiving clinical treatment. The prevalence HFpEF rapidly increasing in the coming decades as global population ages. It becoming clearer that has lot different causes, which makes it challenging to find effective treatments. Currently, there are no proven treatments people deteriorating HF, or HFpEF. Although pathophysiologic foundations complex, excessive reactive oxygen species (ROS) generation and increased oxidative stress caused by mitochondrial dys-function seem play critical role pathogenesis Emerging evidence from an-imal models human myocardial tissues failed hearts shows aberra-tions cause marked increase ROS (mtROS) production stress. Furthermore, studies have reported common HF medications like beta blockers, angioten-sin receptor angiotensin-converting enzyme inhibitors, mineralocorticoid antagonists indirectly reduce mtROS. Despite harmful effects on cardiac remodelling, maintaining homeostasis functions requires small amounts ROS. In this review, we will provide an overview discussion recent findings mtROS production, its threshold imbalance, subsequent dysfunction leads related systemic phenotypes context We also focus newly discovered cellular molecular mechanisms underlying dysregulation, current therapeutic options, future perspectives treating targeting associ-ated signal molecules.
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