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Article ; Online: A global view of the miRNA-mitophagy connexion.

Strappazzon, Flavie

Progress in molecular biology and translational science

2020 Volume 172, Page(s) 37–54

Abstract: Mitochondria are highly dynamics organelles that provide the necessary energy for cellular functions. However, when they are dysfunctional, they can, by contrast, be very harmful for the cell. Mitophagy ensures their recycling and preserves cell ... ...

Abstract	Mitochondria are highly dynamics organelles that provide the necessary energy for cellular functions. However, when they are dysfunctional, they can, by contrast, be very harmful for the cell. Mitophagy ensures their recycling and preserves cell performance. This mechanism is particularly important in neurons because they use a lot of energy. Failed mitophagy can thus affect the development of neurons and lead to brain problems. In this regard, a tight regulation of this process is needed. In recent years microRNAs, as regulators of several biological processes, have attracted attention in the field of mitophagy. In this review, we focused on the studies that highlight the miRNAs implicated in the regulation of mitophagic pathways. In particular, we described the first study carried out 7 years ago, in the context of mitophagy during erythroid differentiation. Next, we have cited all the other works to date on microRNAs and mitophagy regulation. Finally, we have underlined the importance of these discoveries in order to define new therapeutic approaches in the context of age-related diseases involving mitochondrial dysfunctions, such as cancers and neurodegenerative diseases.
Language	English
Publishing date	2020-03-31
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2471995-X
ISSN	1878-0814 ; 0079-6603 ; 1877-1173
ISSN (online)	1878-0814
ISSN	0079-6603 ; 1877-1173
DOI	10.1016/bs.pmbts.2020.03.006
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Article ; Online: A protective variant of the autophagy receptor CALCOCO2/NDP52 in Multiple Sclerosis (MS).

Di Rita, Anthea / Strappazzon, Flavie

Autophagy

2021 Volume 17, Issue 6, Page(s) 1565–1567

Abstract: Multiple sclerosis (MS) is an autoimmune disease of the central nervous system, which has been found associated with dysfunctional mitochondria. In order to advance our understanding of the complex molecular mechanisms underlying this disease, we ... ...

Abstract	Multiple sclerosis (MS) is an autoimmune disease of the central nervous system, which has been found associated with dysfunctional mitochondria. In order to advance our understanding of the complex molecular mechanisms underlying this disease, we analyzed mitophagy, a process fundamental for the elimination of damaged mitochondria through the autophagic process, in peripheral blood mononuclear cells (PBMCs) of MS patients. Through a genetic analysis carried out on 203 MS patients and 1000 healthy controls, we identified a natural variant of CALCOCO2/NDP52, a well-known autophagic receptor, associated with and protective in MS. Structural modeling of the CALCOCO2 variant and functional studies highlighted an amino acid substitution (G140E) located near the LC3-interacting region (LIR) motif of CALCOCO2, crucial in controlling mitophagy. In addition, we found that among PBMCs, CALCOCO2 is mainly expressed in B cells and, by mediating mitophagy, it reduces pro-inflammatory cytokine production following stimulation of these cells. Here we summarize these recent findings, discuss the putative protective roles of CALCOCO2 in B cells and its novel association with an autoimmune disease such as MS.
MeSH term(s)	Autophagy ; Humans ; Leukocytes, Mononuclear ; Mitophagy ; Multiple Sclerosis/genetics ; Nuclear Proteins
Chemical Substances	Nuclear Proteins
Language	English
Publishing date	2021-05-10
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2021.1924969
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Article ; Online: Mitophagy could fight Parkinson's disease through antioxidant action.

Di Rita, Anthea / Strappazzon, Flavie

Reviews in the neurosciences

2019 Volume 30, Issue 7, Page(s) 729–742

Abstract: During aging, the process of mitophagy, a system that allows the removal of dysfunctional mitochondria through lysosomal degradation, starts to malfunction. Because of this defect, damaged mitochondria are not removed correctly, and their decomposing ... ...

Abstract	During aging, the process of mitophagy, a system that allows the removal of dysfunctional mitochondria through lysosomal degradation, starts to malfunction. Because of this defect, damaged mitochondria are not removed correctly, and their decomposing components accumulate inside the cells. Dysfunctional mitochondria that are not removed by mitophagy produce high amounts of reactive oxygen species (ROS) and, thus, cause oxidative stress. Oxidative stress, in turn, is very harmful for the cells, neuronal cells, in particular. Consequently, the process of mitophagy plays a crucial role in mitochondria-related disease. Mitochondrial dysfunctions and oxidative stress are well-established factors contributing to Parkinson's disease (PD), one of the most common neurodegenerative disorders. In this review, we report various known antioxidants for PD treatments and describe the stimulation of mitophagy process as a novel and exciting method for reducing oxidative stress in PD patients. We describe the different mechanisms responsible for mitochondria removal through the mitophagy process. In addition, we review the functional connection between mitophagy induction and reduction of oxidative stress in several
Language	English
Publishing date	2019-03-06
Publishing country	Germany
Document type	Journal Article
ZDB-ID	639035-3
ISSN	2191-0200 ; 0334-1763
ISSN (online)	2191-0200
ISSN	0334-1763
DOI	10.1515/revneuro-2018-0095
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Article: miR-218-5p and doxorubicin combination enhances anticancer activity in breast cancer cells through Parkin-dependent mitophagy inhibition.

Naso, Francesco Davide / Bruqi, Krenare / Manzini, Valeria / Chiurchiù, Valerio / D'Onofrio, Mara / Arisi, Ivan / Strappazzon, Flavie

Cell death discovery

2024 Volume 10, Issue 1, Page(s) 149

Abstract: Breast Cancer (BC) is one of the most common tumours, and is known for its ability to develop resistance to chemotherapeutic treatments. Autophagy has been linked to chemotherapeutic response in several types of cancer, highlighting its contribution to ... ...

Abstract	Breast Cancer (BC) is one of the most common tumours, and is known for its ability to develop resistance to chemotherapeutic treatments. Autophagy has been linked to chemotherapeutic response in several types of cancer, highlighting its contribution to this process. However, the role of mitophagy, a selective form of autophagy responsible for damaged mitochondria degradation, in the response to therapies in BC is still unclear. In order to address this point, we analysed the role of mitophagy in the treatment of the most common anticancer drug, doxorubicin (DXR), in different models of BC, such as a luminal A subtype-BC cell line MCF7 cells, cultured in 2-Dimension (2D) or in 3-Dimension (3D), and the triple negative BC (TNBC) cell line MDA-MB-231. Through a microarray analysis, we identified a relationship between mitophagy gene expressions related to the canonical PINK1/Parkin-mediated pathway and DXR treatment in BC cells. Afterwards, we demonstrated that the PINK1/Parkin-dependent mitophagy is indeed induced following DXR treatment and that exogenous expression of a small non-coding RNA, the miRNA-218-5p, known to target mRNA of Parkin, was sufficient to inhibit the DXR-mediated mitophagy in MCF7 and in MDA-MB-231 cells, thereby increasing their sensitivity to DXR. Considering the current challenges involved in BC refractory to treatment, our work could provide a promising approach to prevent tumour resistance and recurrence, potentially leading to the development of an innovative approach to combine mitophagy inhibition and chemotherapy.
Language	English
Publishing date	2024-03-21
Publishing country	United States
Document type	Journal Article
ISSN	2058-7716
ISSN	2058-7716
DOI	10.1038/s41420-024-01914-7
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Article ; Online: Mitophagy and iron: two actors sharing the stage in age-associated neuronal pathologies.

Schiavi, Alfonso / Strappazzon, Flavie / Ventura, Natascia

Mechanisms of ageing and development

2020 Volume 188, Page(s) 111252

Abstract: Aging is characterized by the deterioration of different cellular and organismal structures and functions. A typical hallmark of the aging process is the accumulation of dysfunctional mitochondria and excess iron, leading to a vicious cycle that promotes ...

Abstract	Aging is characterized by the deterioration of different cellular and organismal structures and functions. A typical hallmark of the aging process is the accumulation of dysfunctional mitochondria and excess iron, leading to a vicious cycle that promotes cell and tissue damage, which ultimately contribute to organismal aging. Accordingly, altered mitochondrial quality control pathways such as mitochondrial autophagy (mitophagy) as well as altered iron homeostasis, with consequent iron overload, can accelerate the aging process and the development and progression of different age-associated disorders. In this review we first briefly introduce the aging process and summarize molecular mechanisms regulating mitophagy and iron homeostasis. We then provide an overview on how dysfunction of these two processes impact on aging and age-associated neurodegenerative disorders with a focus on Alzheimer's disease, Parkinson's disease and Amyotrophic Lateral Sclerosis. Finally, we summarize some recent evidence showing mechanistic links between iron metabolism and mitophagy and speculate on how regulating the crosstalk between the two processes may provide protective effects against aging and age-associated neuronal pathologies.
MeSH term(s)	Aging ; Alzheimer Disease/metabolism ; Animals ; Autophagy/physiology ; Cardiovascular Diseases/metabolism ; Heart Failure/metabolism ; Homeostasis ; Humans ; Iron/metabolism ; Lysosomes/metabolism ; Mitochondria/metabolism ; Mitophagy/physiology ; Neurons/metabolism ; Oxygen/metabolism ; Parkinson Disease/metabolism ; Phosphorylation
Chemical Substances	Iron (E1UOL152H7) ; Oxygen (S88TT14065)
Language	English
Publishing date	2020-04-21
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	183915-9
ISSN	1872-6216 ; 0047-6374
ISSN (online)	1872-6216
ISSN	0047-6374
DOI	10.1016/j.mad.2020.111252
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Article: AMBRA1-induced mitophagy: A new mechanism to cope with cancer?

Strappazzon, Flavie / Cecconi, Francesco

Molecular & cellular oncology

2015 Volume 2, Issue 2, Page(s) e975647

Abstract: Dysfunctions in mitophagy, the process by which mitochondria are eliminated, are associated with cancer. We found that the proautophagic protein AMBRA1 (activating molecule in beclin 1 regulated autophagy) binds the autophagosome adapter LC3, and that ... ...

Abstract	Dysfunctions in mitophagy, the process by which mitochondria are eliminated, are associated with cancer. We found that the proautophagic protein AMBRA1 (activating molecule in beclin 1 regulated autophagy) binds the autophagosome adapter LC3, and that this interaction is crucial for mitochondrial clearance with or without involvement of the E3-ligase PARKIN. The discovery of a novel mitophagy pathway has the potential to promote new anticancer strategies.
Language	English
Publishing date	2015-02-25
Publishing country	United States
Document type	Journal Article
ISSN	2372-3556
ISSN	2372-3556
DOI	10.4161/23723556.2014.975647
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Article: Cobalt chloride has beneficial effects across species through a hormetic mechanism.

Schiavi, Alfonso / Runci, Alessandra / Maiorino, Teresa / Naso, Francesco Davide / Barenys, Marta / Fritsche, Ellen / Strappazzon, Flavie / Ventura, Natascia

Frontiers in cell and developmental biology

2022 Volume 10, Page(s) 986835

Abstract: Severe oxygen and iron deficiencies have evolutionarily conserved detrimental effects, leading to pathologies in mammals and developmental arrest as well as neuromuscular degeneration in the ... ...

Abstract	Severe oxygen and iron deficiencies have evolutionarily conserved detrimental effects, leading to pathologies in mammals and developmental arrest as well as neuromuscular degeneration in the nematode
Language	English
Publishing date	2022-10-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2022.986835
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Article ; Online: The multifaceted mitochondrion: An attractive candidate for therapeutic strategies.

Strappazzon, Flavie / Cecconi, Francesco

Pharmacological research

2015 Volume 99, Page(s) 425–433

Abstract: Mitochondria are considered the powerhouse of the cell and disturbances in mitochondrial functions are involved in several disorders such as neurodegeneration and mitochondrial diseases. This review summarizes pharmacological strategies that aim at ... ...

Abstract	Mitochondria are considered the powerhouse of the cell and disturbances in mitochondrial functions are involved in several disorders such as neurodegeneration and mitochondrial diseases. This review summarizes pharmacological strategies that aim at modifying the number of mitochondria, their dynamics or the mitochondrial quality-control mechanisms, in several pathological instances in which any of these mechanisms are impaired or abnormal. The interplay between different cellular pathways that involve mitochondria in order to respond to stress is highlighted. Such a high mitochondrial plasticity could be exploited for new treatments.
MeSH term(s)	Animals ; Humans ; Mitochondria/physiology ; Mitochondrial Diseases/pathology ; Neurodegenerative Diseases/pathology ; Signal Transduction/physiology
Language	English
Publishing date	2015-03-24
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1003347-6
ISSN	1096-1186 ; 0031-6989 ; 1043-6618
ISSN (online)	1096-1186
ISSN	0031-6989 ; 1043-6618
DOI	10.1016/j.phrs.2015.03.007
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Article ; Online: miR-218 Inhibits Mitochondrial Clearance by Targeting PRKN E3 Ubiquitin Ligase.

Di Rita, Anthea / Maiorino, Teresa / Bruqi, Krenare / Volpicelli, Floriana / Bellenchi, Gian Carlo / Strappazzon, Flavie

International journal of molecular sciences

2020 Volume 21, Issue 1

Abstract: The selective elimination of dysfunctional mitochondria through mitophagy is crucial for preserving mitochondrial quality and cellular homeostasis. The most described mitophagy pathway is regulated by a positive ubiquitylation feedback loop in which the ... ...

Abstract	The selective elimination of dysfunctional mitochondria through mitophagy is crucial for preserving mitochondrial quality and cellular homeostasis. The most described mitophagy pathway is regulated by a positive ubiquitylation feedback loop in which the PINK1 (PTEN induced kinase 1) kinase phosphorylates both ubiquitin and the E3 ubiquitin ligase PRKN (Parkin RBR E3 ubiquitin ligase), also known as PARKIN. This event recruits PRKN to the mitochondria, thus amplifying ubiquitylation signal. Here we report that miR-218 targets PRKN and negatively regulates PINK1/PRKN-mediated mitophagy. Overexpression of miR-218 reduces PRKN mRNA levels, thus also reducing protein content and deregulating the E3 ubiquitin ligase action. In fact, following miR-218 overexpression, mitochondria result less ubiquitylated and the autophagy machinery fails to proceed with correct mitochondrial clearance. Since mitophagy defects are associated with various human diseases, these results qualify miR-218 as a promising therapeutic target for human diseases.
MeSH term(s)	Autophagosomes/metabolism ; HEK293 Cells ; Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitophagy/genetics ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism
Chemical Substances	MIRN218 microRNA, human ; MicroRNAs ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; parkin protein (EC 2.3.2.27)
Language	English
Publishing date	2020-01-05
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21010355
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Article ; Online: MIR7-3HG, a MYC-dependent modulator of cell proliferation, inhibits autophagy by a regulatory loop involving AMBRA1.

Capizzi, Mariacristina / Strappazzon, Flavie / Cianfanelli, Valentina / Papaleo, Elena / Cecconi, Francesco

Autophagy

2017 Volume 13, Issue 3, Page(s) 554–566

Abstract: Macroautophagy/autophagy is a tightly regulated intracellular catabolic pathway involving the lysosomal degradation of cytoplasmic organelles and proteins to be recycled into metabolic precursors. AMBRA1 (autophagy and Beclin 1 regulator 1) has a central ...

Abstract	Macroautophagy/autophagy is a tightly regulated intracellular catabolic pathway involving the lysosomal degradation of cytoplasmic organelles and proteins to be recycled into metabolic precursors. AMBRA1 (autophagy and Beclin 1 regulator 1) has a central role in the autophagy signaling network; it acts upstream of MTORC1-dependent autophagy by stabilizing the kinase ULK1 (unc-51 like autophagy activating kinase 1) and by favoring autophagosome core complex formation. AMBRA1 also regulates the cell cycle by modulating the activity of the phosphatase PPP2/PP2A (protein phosphatase 2) and degradation of MYC. Of note, post-transcriptional regulation mediated by noncoding microRNAs (MIRNAs) contributes significantly to control autophagy. Here we describe a new role for the microRNA MIR7-3HG/MIR-7 as a potent autophagy inhibitor. Indeed, MIR7-3HG targets the 3' untranslated region (UTR) of AMBRA1 mRNA, inducing a decrease of both AMBRA1 mRNA and protein levels, and thus causing a block in autophagy. Furthermore, MIR7-3HG, through AMBRA1 downregulation, prevents MYC dephosphorylation, establishing a positive feedback for its own transcription. These data suggest a new and interesting role of MIR7-3HG as an anti-autophagic MIRNA that may affect oncogenesis through the regulation of the tumor suppressor AMBRA1.
Language	English
Publishing date	2017-03-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2016.1269989
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