Mitophagy, Mitochondrial Dynamics, and Homeostasis in Cardiovascular Aging

Wu, Ne N.; Zhang, Yingmei; Ren, Jun

doi:10.1155/2019/9825061

Cited by 155 publications

(117 citation statements)

References 175 publications

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“…Upon nutrient starvation, mTORC1 is inactivated, thus relieving the inhibition of phosphorylation of ULK1-Atg13-FIP200 complex. In cardiac aging, the modulation of autophagy involves AMP-activated protein kinase (AMPK) [2]. Activated AMPK turns on autophagy though the inhibition of mTOR and redirects metabolism towards increased catabolism and decreased anabolism.…”

Section: Autophagy In Cardiacmentioning

confidence: 99%

“…An imbalance between fission and fusion is detrimental to mitochondrial homeostasis and mitochondrial quality [2]. Hence, addressing this unfavorable situation is a vital issue.…”

Section: Mitochondrial Dysfunction In Cardiac Agingmentioning

confidence: 99%

“…Age is widely recognized as the leading risk factor for CVDs. Cardiac aging is defined as the gradual deterioration of cardiac structure and function with age [2]. Diastolic dysfunction and left ventricular hypertrophy often occur in the elderly.…”

Section: Introductionmentioning

confidence: 99%

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Mitochondrial ROS-Modulated mtDNA: A Potential Target for Cardiac Aging

Quan

Xin

Tian

et al. 2020

Oxidative Medicine and Cellular Longevity

134

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Mitochondrial DNA (mtDNA) damage is associated with the development of cardiovascular diseases. Cardiac aging plays a central role in cardiovascular diseases. There is accumulating evidence linking cardiac aging to mtDNA damage, including mtDNA mutation and decreased mtDNA copy number. Current wisdom indicates that mtDNA is susceptible to damage by mitochondrial reactive oxygen species (mtROS). This review presents the cellular and molecular mechanisms of cardiac aging, including autophagy, chronic inflammation, mtROS, and mtDNA damage, and the effects of mitochondrial biogenesis and oxidative stress on mtDNA. The importance of nucleoid-associated proteins (Pol γ), nuclear respiratory factors (NRF1 and NRF2), the cGAS-STING pathway, and the mitochondrial biogenesis pathway concerning the development of mtDNA damage during cardiac aging is discussed. Thus, the repair of damaged mtDNA provides a potential clinical target for preventing cardiac aging.

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Section: Autophagy In Cardiacmentioning

confidence: 99%

“…An imbalance between fission and fusion is detrimental to mitochondrial homeostasis and mitochondrial quality [2]. Hence, addressing this unfavorable situation is a vital issue.…”

Section: Mitochondrial Dysfunction In Cardiac Agingmentioning

confidence: 99%

See 1 more Smart Citation

Mitochondrial ROS-Modulated mtDNA: A Potential Target for Cardiac Aging

Quan

Xin

Tian

et al. 2020

Oxidative Medicine and Cellular Longevity

134

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“…Defective mitophagy causes a pronounced accumulation of damaged mitochondria and excessive inflammation caused by pro-inflammatory cytokines [80]. Mitophagy, in turn, is dependent on a correct balance between mitochondrial fission and fusion processes [81]. Mitochondrial fission ensures effective mitophagy, while fusion contributes to biogenesis and restoration of the organelles.…”

Section: Innate Immunity and Mitochondrial Dysfunctionmentioning

confidence: 99%

Possible Role of Mitochondrial DNA Mutations in Chronification of Inflammation: Focus on Atherosclerosis

Orekhov

Nikiforov

Ivanova

et al. 2020

JCM

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Chronification of inflammation is the process that lies at the basis of several human diseases that make up to 80% of morbidity and mortality worldwide. It can also explain a great deal of processes related to aging. Atherosclerosis is an example of the most important chronic inflammatory pathology in terms of public health impact. Atherogenesis is based on the inflammatory response of the innate immunity arising locally or focally. The main trigger for this response appears to be modified low-density lipoprotein (LDL), although other factors may also play a role. With the quick resolution of inflammation, atherosclerotic changes in the arterial wall do not occur. However, a violation of the innate immunity response can lead to chronification of local inflammation and, as a result, to atherosclerotic lesion formation. In this review, we discuss possible mechanisms of the impaired immune response with a special focus on mitochondrial dysfunction. Some mitochondrial dysfunctions may be due to mutations in mitochondrial DNA. Several mitochondrial DNA mutations leading to defective mitophagy have been identified. The regulatory role of mitophagy in the immune response has been shown in recent studies. We suggest that defective mitophagy promoted by mutations in mitochondrial DNA can cause innate immunity disorders leading to chronification of inflammation.

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“…Indeed, senescent cells display altered mitochondrial dynamics and loss of membrane potential (21). Interestingly enough, overexpression of proteins involved in the autophagosome formation (ATG5 and ATG12) was associated with improved mitochondrial performance, as evidenced by higher membrane potential, increased ATP production, and decreased damage to mtDNA (22,23).…”

mentioning

confidence: 99%

Epigenetic Control of Mitochondrial Function in the Vasculature

Mohammed

Ambrosini

Lüscher

et al. 2020

Front. Cardiovasc. Med.

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The molecular signatures of epigenetic regulation and chromatin architecture are emerging as pivotal regulators of mitochondrial function. Recent studies unveiled a complex intersection among environmental factors, epigenetic signals, and mitochondrial metabolism, ultimately leading to alterations of vascular phenotype and increased cardiovascular risk. Changing environmental conditions over the lifetime induce covalent and post-translational chemical modification of the chromatin template which sensitize the genome to establish new transcriptional programs and, hence, diverse functional states. On the other hand, metabolic alterations occurring in mitochondria affect the availability of substrates for chromatin-modifying enzymes, thus leading to maladaptive epigenetic signatures altering chromatin accessibility and gene transcription. Indeed, several components of the epigenetic machinery require intermediates of cellular metabolism (ATP, AcCoA, NADH, α-ketoglutarate) for enzymatic function. In the present review, we describe the emerging role of epigenetic modifications as fine tuners of gene transcription in mitochondrial dysfunction and vascular disease. Specifically, the following aspects are described in detail: (i) mitochondria and vascular function, (ii) mitochondrial ROS, (iii) epigenetic regulation of mitochondrial function; (iv) the role of mitochondrial metabolites as key effectors for chromatin-modifying enzymes; (v) epigenetic therapies. Understanding epigenetic routes may pave the way for new approaches to develop personalized therapies to prevent mitochondrial insufficiency and its complications.

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Mitophagy, Mitochondrial Dynamics, and Homeostasis in Cardiovascular Aging

Cited by 155 publications

References 175 publications

Mitochondrial ROS-Modulated mtDNA: A Potential Target for Cardiac Aging

Mitochondrial ROS-Modulated mtDNA: A Potential Target for Cardiac Aging

Possible Role of Mitochondrial DNA Mutations in Chronification of Inflammation: Focus on Atherosclerosis

Epigenetic Control of Mitochondrial Function in the Vasculature

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