Regulation of mitochondrial cargo-selective autophagy by posttranslational modifications

Terradas, Anna Lechado; Zittlau, Katharina; Maček, Boris; Fraiberg, Milana; Elazar, Zvulun; Kahle, Philipp J.

doi:10.1016/j.jbc.2021.101339

Cited by 12 publications

(4 citation statements)

References 202 publications

(291 reference statements)

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“…As we explain above, fasting induces an ANTI-Warburg effect ( Bianchi et al, 2015 ; Choi et al, 2016 ; Mattson et al, 2017 ; de Cabo and Mattson, 2019 ; Kornberg, 2020 ; Locati et al, 2020 ; Cuevas-Cervera et al, 2022 ) and prevents pathological accumulation or altered proteostasis that are part of the pathophysiology pathways leading to neurological and metabolic pathologies. Protein and biomass accumulation is treatable, improving autophagia, for example, with fasting ( Gherardi et al, 2019 ; Hu et al, 2021 ; Lechado Terradas et al, 2021 ; Lizama and Chu, 2021 ; Roberts and Markby, 2021 ).…”

Section: Part Iii: Strategies To Restore the Mitochondria As A Therap...mentioning

confidence: 99%

Mitochondria: It is all about energy

et al. 2023

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Mitochondria play a key role in both health and disease. Their function is not limited to energy production but serves multiple mechanisms varying from iron and calcium homeostasis to the production of hormones and neurotransmitters, such as melatonin. They enable and influence communication at all physical levels through interaction with other organelles, the nucleus, and the outside environment. The literature suggests crosstalk mechanisms between mitochondria and circadian clocks, the gut microbiota, and the immune system. They might even be the hub supporting and integrating activity across all these domains. Hence, they might be the (missing) link in both health and disease. Mitochondrial dysfunction is related to metabolic syndrome, neuronal diseases, cancer, cardiovascular and infectious diseases, and inflammatory disorders. In this regard, diseases such as cancer, Alzheimer’s, Parkinson’s, amyotrophic lateral sclerosis (ALS), chronic fatigue syndrome (CFS), and chronic pain are discussed. This review focuses on understanding the mitochondrial mechanisms of action that allow for the maintenance of mitochondrial health and the pathways toward dysregulated mechanisms. Although mitochondria have allowed us to adapt to changes over the course of evolution, in turn, evolution has shaped mitochondria. Each evolution-based intervention influences mitochondria in its own way. The use of physiological stress triggers tolerance to the stressor, achieving adaptability and resistance. This review describes strategies that could recover mitochondrial functioning in multiple diseases, providing a comprehensive, root-cause-focused, integrative approach to recovering health and treating people suffering from chronic diseases.

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Section: Part Iii: Strategies To Restore the Mitochondria As A Therap...mentioning

confidence: 99%

Mitochondria: It is all about energy

et al. 2023

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“…6 B) ( e.g ., –OH, –SH or –NH 2 ) on its side chain. In fact, a significant number of post-translational modifications (PTMs) occur in autophagy regulation 141 , 142 , 143 , 144 , 145 . Those PTMs on the PPI interface of interest imply that chemical modifications on those relevant residues are potentially favored.…”

Section: General Strategies For Obtaining Protein–protein Interaction...mentioning

confidence: 99%

Drug discovery by targeting the protein–protein interactions involved in autophagy

Xiang

Zhou

et al. 2023

Acta Pharmaceutica Sinica B

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“…Indeed, elamipretide or CoQ10 reduced kidney injury in experimental type 1 (streptozotocin) and type 2 (db/db mice) diabetes ( Table 2 ) [ 90 , 91 , 92 ]. Post-translational modifications of mitochondrial proteins may also alter mitochondria function and biogenesis [ 93 , 94 ]. Increased nitrotyrosine staining in the kidneys of streptozotocin-induced T1D in ApoE -/- mice was associated with reduced manganese SOD activity [ 95 ].…”

Section: Mitochondrial Dysfunction and Oxidative Stress In Ckdmentioning

confidence: 99%

Tubular Mitochondrial Dysfunction, Oxidative Stress, and Progression of Chronic Kidney Disease

et al. 2022

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Acute kidney injury (AKI) and chronic kidney disease (CKD) are interconnected conditions, and CKD is projected to become the fifth leading global cause of death by 2040. New therapeutic approaches are needed. Mitochondrial dysfunction and oxidative stress have emerged as drivers of kidney injury in acute and chronic settings, promoting the AKI-to-CKD transition. In this work, we review the role of mitochondrial dysfunction and oxidative stress in AKI and CKD progression and discuss novel therapeutic approaches. Specifically, evidence for mitochondrial dysfunction in diverse models of AKI (nephrotoxicity, cytokine storm, and ischemia-reperfusion injury) and CKD (diabetic kidney disease, glomerulopathies) is discussed; the clinical implications of novel information on the key role of mitochondria-related transcriptional regulators peroxisome proliferator-activated receptor gamma coactivator 1-alpha, transcription factor EB (PGC-1α, TFEB), and carnitine palmitoyl-transferase 1A (CPT1A) in kidney disease are addressed; the current status of the clinical development of therapeutic approaches targeting mitochondria are updated; and barriers to the clinical development of mitochondria-targeted interventions are discussed, including the lack of clinical diagnostic tests that allow us to categorize the baseline renal mitochondrial dysfunction/mitochondrial oxidative stress and to monitor its response to therapeutic intervention. Finally, key milestones for further research are proposed.

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Regulation of mitochondrial cargo-selective autophagy by posttranslational modifications

Cited by 12 publications

References 202 publications

Mitochondria: It is all about energy

Mitochondria: It is all about energy

Drug discovery by targeting the protein–protein interactions involved in autophagy

Tubular Mitochondrial Dysfunction, Oxidative Stress, and Progression of Chronic Kidney Disease

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