Mitochondria, a Missing Link in COVID-19 Heart Failure and Arrest?

Ryback, Ralph S.; Eirin, Alfonso

doi:10.3389/fcvm.2021.830024

Cited by 10 publications

(9 citation statements)

References 25 publications

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“…The mitochondrial impact of SARS-CoV-2 infection is a topic gaining traction as experimental data on dysfunctional mitochondrial metabolism and transcriptome have been accumulating [ 66 ]. Cardiac cells have high ATP needs, and their activity heavily relies on mitochondrial health [ 67 ].…”

Section: Discussionmentioning

confidence: 99%

Gene Network Analysis of the Transcriptome Impact of SARS-CoV-2 Interacting MicroRNAs in COVID-19 Disease

Moatăr

Chis

Marian

et al. 2022

IJMS

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According to the World Health Organization (WHO), as of June 2022, over 536 million confirmed COVID-19 disease cases and over 6.3 million deaths had been globally reported. COVID-19 is a multiorgan disease involving multiple intricated pathological mechanisms translated into clinical, biochemical, and molecular changes, including microRNAs. MicroRNAs are essential post-transcriptional regulators of gene expression, being involved in the modulation of most biological processes. In this study, we characterized the biological impact of SARS-CoV-2 interacting microRNAs differentially expressed in COVID-19 disease by analyzing their impact on five distinct tissue transcriptomes. To this end, we identified the microRNAs’ predicted targets within the list of differentially expressed genes (DEGs) in tissues affected by high loads of SARS-CoV-2 virus. Next, we submitted the tissue-specific lists of the predicted microRNA-targeted DEGs to gene network functional enrichment analysis. Our data show that the upregulated microRNAs control processes such as mitochondrial respiration and cytokine and cell surface receptor signaling pathways in the heart, lymph node, and kidneys. In contrast, downregulated microRNAs are primarily involved in processes related to the mitotic cell cycle in the heart, lung, and kidneys. Our study provides the first exploratory, systematic look into the biological impact of the microRNAs associated with COVID-19, providing a new perspective for understanding its multiorgan physiopathology.

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Section: Discussionmentioning

confidence: 99%

Gene Network Analysis of the Transcriptome Impact of SARS-CoV-2 Interacting MicroRNAs in COVID-19 Disease

Moatăr

Chis

Marian

et al. 2022

IJMS

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“…121 Cardiac mitochondrial damage that leads to heart failure and cardiac arrest has been reported as a consequence of SARS-CoV-2 infection, possibly by altering mitochondrial homeostasis, leading to apoptosis, inducing ROS, and reducing ATP production and autophagy. 122 A high level of degraded mitochondria in blood has been reported as a prediction of poor COVID-19 outcome. 122 It was previously reported that SARS-CoV-2 might enter the host cell via the angiotensin-converting enzyme carboxypeptidase 2 (ACE2) and subsequently manipulate host mitochondria by viral openreading frames, which results in the release of mtDNA into the cytoplasm and consequently induces the formation of inflammasome and suppresses innate and adaptive immunity.…”

Section: Mitochondria and Covid-19/long Covidmentioning

confidence: 99%

The Role of Mitochondria in Phytochemically Mediated Disease Amelioration

Koh

Pan

2023

J. Agric. Food Chem.

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Mitochondrial dysfunction may cause cell death, which has recently emerged as a cancer prevention and treatment strategy mediated by chemotherapy drugs or phytochemicals. However, most existing drugs cannot target cancerous cells and may adversely affect normal cells via side effects. Mounting studies have revealed that phytochemicals such as resveratrol could ameliorate various diseases with dysfunctional or damaged mitochondria. For instance, resveratrol can regulate mitophagy, inhibit oxidative stress and preserve membrane potential, induce mitochondrial biogenesis, balance mitochondrial fusion and fission, and enhance the functionality of the electron transport chain. However, there are only a few studies suggesting that phytochemicals could potentially protect against the cytotoxicity of some current cancer drugs, especially those that damage mitochondria. Besides, COVID-19 and long COVID have also been reported to be correlated to mitochondrial dysfunction. Curcumin has been reported bringing a positive impact on COVID-19 and long COVID. Therefore, in this study, the benefits of resveratrol and curcumin to be applied for cancer treatment/prevention and disease amelioration were reviewed. Besides, this review also provides some perspectives on phytochemicals to be considered as a treatment adjuvant for COVID-19 and long COVID by targeting mitochondrial rescue. Hopefully, this review can provide new insight into disease treatment with phytochemicals targeting mitochondria.

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“…Mitochondria are substantial organelles that maintain the structure and function of the heart. [8][9][10] Moderate exercise could induce increased mitochondrial number and function in cardiomyocytes, 35 while strenuous exercise resulted in mitochondrial disturbance coupled with cardiac abnormalities, [15][16][17] suggesting that the modulation of mitochondrial homeostasis may occupy a critical position in the transition from exercise-related physiological hypertrophy to pathological hypertrophy. Of note, recent evidence reported that the PGC-1α mRNA level was negatively correlated with the exercise intensity, 36 which indicated that PGC-1α-mediated mitochondrial biogenesis, a pivotal aspect in maintaining mitochondrial homeostasis, may be "exercise intensity-sensitive".…”

Section: Papermentioning

confidence: 99%

“…Mitochondrial homeostasis, which indicates the balanced and healthy status of mitochondrial biogenesis, mitochondrial dynamics, mitophagy, etc., occupies a critical position in maintaining normal cardiac function. [8][9][10] Moderate exercise has been demonstrated to exert its benefits by promoting mitochondrial biogenesis and enhancing mitochondrial function, 11,12 whereas prolonged strenuous exercise is reported to be coupled with mitochondrial disturbance. [13][14][15] Of note, recent evidence revealed a possible correlation between loss of mitochondrial homeostasis and the development of strenuous exercise-induced cardiac abnormalities.…”

Section: Introductionmentioning

confidence: 99%