Mitochondrial autophagy: molecular mechanisms and implications for cardiovascular disease

Li, Anqi; Gao, Meng; Liu, Bilin; Qin, Yuan; Chen, Lei; Liu, Hanyu; Wu, Haoyue; Gong, Guohua

doi:10.1038/s41419-022-04906-6

Cited by 162 publications

(86 citation statements)

References 185 publications

(198 reference statements)

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“…Of note, mitophagy is pivotal for mitochondrial quality control and plays a dual role in the progression of diverse CVDs. The emerging role of alternative forms of mitophagy in CVDs is well summarized in Pedro, Morales, and Li's studies [13,208,209]. However, since the current studies are mainly focused on the role of mitophagy in cardiomyocytes, vascular smooth muscle cells, and ECs in the aorta, their roles in coronary ECs are less mentioned and further studies are warranted.…”

Section: Discussionmentioning

confidence: 95%

Endothelial Autophagy in Coronary Microvascular Dysfunction and Cardiovascular Disease

Zhao

Satyanarayana

Zhang

et al. 2022

Cells

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Coronary microvascular dysfunction (CMD) refers to a subset of structural and/or functional disorders of coronary microcirculation that lead to impaired coronary blood flow and eventually myocardial ischemia. Amid the growing knowledge of the pathophysiological mechanisms and the development of advanced tools for assessment, CMD has emerged as a prevalent cause of a broad spectrum of cardiovascular diseases (CVDs), including obstructive and nonobstructive coronary artery disease, diabetic cardiomyopathy, and heart failure with preserved ejection fraction. Of note, the endothelium exerts vital functions in regulating coronary microvascular and cardiac function. Importantly, insufficient or uncontrolled activation of endothelial autophagy facilitates the pathogenesis of CMD in diverse CVDs. Here, we review the progress in understanding the pathophysiological mechanisms of autophagy in coronary endothelial cells and discuss their potential role in CMD and CVDs.

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Section: Discussionmentioning

confidence: 95%

Endothelial Autophagy in Coronary Microvascular Dysfunction and Cardiovascular Disease

Zhao

Satyanarayana

Zhang

et al. 2022

Cells

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“…Dysfunctional or superfluous mitochondria can be degraded via bulk autophagy or mitochondria-specific autophagy (mitophagy) ( Figure 2 box 5) ( Li et al, 2022 ). Mutations in mitophagy regulators, such as PTEN-induced putative kinase 1 (PINK1) and the cytosolic E3 ligase Parkin, are known as causal genes for familiar Parkinson disease ( Kitada et al, 1998 ; Valente et al, 2004 ; Narendra et al, 2010 ).…”

Section: Mitochondrial Maintenance: Mitochondrial Dynamics Clearance ...mentioning

confidence: 99%

Dynamic features of human mitochondrial DNA maintenance and transcription

Akbari

Nilsen

Montaldo

2022

Front. Cell Dev. Biol.

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Mitochondria are the primary sites for cellular energy production and are required for many essential cellular processes. Mitochondrial DNA (mtDNA) is a 16.6 kb circular DNA molecule that encodes only 13 gene products of the approximately 90 different proteins of the respiratory chain complexes and an estimated 1,200 mitochondrial proteins. MtDNA is, however, crucial for organismal development, normal function, and survival. MtDNA maintenance requires mitochondrially targeted nuclear DNA repair enzymes, a mtDNA replisome that is unique to mitochondria, and systems that control mitochondrial morphology and quality control. Here, we provide an overview of the current literature on mtDNA repair and transcription machineries and discuss how dynamic functional interactions between the components of these systems regulate mtDNA maintenance and transcription. A profound understanding of the molecular mechanisms that control mtDNA maintenance and transcription is important as loss of mtDNA integrity is implicated in normal process of aging, inflammation, and the etiology and pathogenesis of a number of diseases.

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“…Monitoring ATP dysregulation can provide diagnostic information for cardiovascular, neurodegenerative, and mitochondrial diseases, hypoxia, hypoglycemia, ischemia, and the progression, invasiveness, and drug resistance of malignant tumors. [36][37][38][39][40][41][42][43] Therefore, accurate detection and quantification of ATP are highly important to understand biological systems and improve diagnosis and treatment. Luciferase-based approaches for ATP detection are a workhorse in molecular biology, with good sensitivity for quantification from cell lysates.…”

Section: Introductionmentioning

confidence: 99%

CRISPR/Cas-assisted Nanoneedle Sensor for ATP Detection in Living Cells

Kim

Mustfa

et al. 2022

Preprint

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The clustered regularly interspaced short palindromic repeats (CRISPR)-associated protein (Cas) (CRISPR/Cas) systems have recently emerged as a powerful molecular biosensing tool based on their collateral cleavage activity due to their simplicity, sensitivity, specificity, and broad applicability. However, the direct application of collateral cleavage activity for in-situ intracellular detection is still challenging. Here, we debut a CRISPR/Cas-assisted nanoneedle sensor (nanoCRISPR) for intracellular adenosine triphosphate (ATP), which avoids the challenges associated with intracellular collateral cleavage by introducing a two-step process of intracellular target recognition followed by extracellular transduction and detection. ATP recognition occurs by first presenting in the cell cytosol an aptamer-locked Cas12a activator conjugated to nanoneedles; the recognition event unlocks the activator immobilized on the nanoneedles. The nanoneedles are then removed from the cells and exposed to the Cas12a/crRNA complex, where the activator triggers the cleavage of a ssDNA fluorophore-quencher pair, generating a detectable fluorescence signal. NanoCRISPR has an ATP detection limit of 246 nM and a dynamic range from 1.56 μM to 50 μM. Importantly, nanoCRISPR can detect intracellular ATP in 30 min in live cells without impacting cell viability. We anticipate that the nanoCRISPR approach will contribute to broaden the biomedical applications of CRISPR/Cas sensors for the detection of diverse intracellular molecules in living systems.

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Mitochondrial autophagy: molecular mechanisms and implications for cardiovascular disease

Cited by 162 publications

References 185 publications

Endothelial Autophagy in Coronary Microvascular Dysfunction and Cardiovascular Disease

Endothelial Autophagy in Coronary Microvascular Dysfunction and Cardiovascular Disease

Dynamic features of human mitochondrial DNA maintenance and transcription

CRISPR/Cas-assisted Nanoneedle Sensor for ATP Detection in Living Cells

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