Interorganellar calcium signaling in the regulation of cell metabolism: A cancer perspective

Rimessi, Alessandro; Pedriali, Gaia; Vezzani, Bianca; Tarocco, Anna; Marchi, Saverio; Wieckowski, Mariusz R.; Giorgi, Carlotta; Pinton, Paolo

doi:10.1016/j.semcdb.2019.05.015

Cited by 37 publications

(29 citation statements)

References 242 publications

(266 reference statements)

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“…For instance, in H-Ras-transformed fibroblasts, CAV1 re-expression promotes Ca 2+ reentry, thus making them prone to cell death [137]. Indeed, any alteration to the CAV1/Ca 2+ axis triggers mitochondrial dysfunction and apoptosis in transformed cells [137,138]. Interestingly, however, CAV1 has also been shown to promote tumor development by regulating Ca 2+ homeostasis in breast, stomach, lung, colon, and liver cancers [138].…”

Section: Cav1 Localization In Mitochondria-associated Membranesmentioning

confidence: 99%

Caveolin-1 function at the plasma membrane and in intracellular compartments in cancer

Simón

Campos

Leyton

et al. 2020

Cancer Metastasis Rev

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Caveolin-1 (CAV1) is commonly considered to function as a cell surface protein, for instance in the genesis of caveolae. Nonetheless, it is also present in many intracellular organelles and compartments. The contributions of these intracellular pools to CAV1 function are generally less well understood, and this is also the case in the context of cancer. This review will summarize literature available on the role of CAV1 in cancer, highlighting particularly our understanding of the canonical (CAV1 in the plasma membrane) and non-canonical pathways (CAV1 in organelles and exosomes) linked to the dual role of the protein as a tumor suppressor and promoter of metastasis. With this in mind, we will focus on recently emerging concepts linking CAV1 function to the regulation of intracellular organelle communication within the same cell where CAV1 is expressed. However, we now know that CAV1 can be released from cells in exosomes and generate systemic effects. Thus, we will also elaborate on how CAV1 participates in intracellular communication between organelles as well as signaling between cells (non-canonical pathways) in cancer.

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Section: Cav1 Localization In Mitochondria-associated Membranesmentioning

confidence: 99%

Caveolin-1 function at the plasma membrane and in intracellular compartments in cancer

Simón

Campos

Leyton

et al. 2020

Cancer Metastasis Rev

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“…The loss of ΔΨm leads to a retrograde response, in which mitochondria regulate several signal transduction proteins to control stress-responsive genes in the nucleus [ 64 ]. Mitochondrial coupling is strictly related to ATP production, ROS generation and Ca 2+ homeostasis, and all these processes are finely tuned to maintain physiological conditions [ 65 , 66 ]. Given their importance, mitochondria have crucial roles in the pathophysiology of several cardiovascular diseases.…”

Section: Aortic Stenosis Pathobiology a Molecular Perspectivementioning

confidence: 99%

Aortic Valve Stenosis and Mitochondrial Dysfunctions: Clinical and Molecular Perspectives

Pedriali

Morciano

Patergnani

et al. 2020

IJMS

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Calcific aortic stenosis is a disorder that impacts the physiology of heart valves. Fibrocalcific events progress in conjunction with thickening of the valve leaflets. Over the years, these events promote stenosis and obstruction of blood flow. Known and common risk factors are congenital defects, aging and metabolic syndromes linked to high plasma levels of lipoproteins. Inflammation and oxidative stress are the main molecular mediators of the evolution of aortic stenosis in patients and these mediators regulate both the degradation and remodeling processes. Mitochondrial dysfunction and dysregulation of autophagy also contribute to the disease. A better understanding of these cellular impairments might help to develop new ways to treat patients since, at the moment, there is no effective medical treatment to diminish neither the advancement of valve stenosis nor the left ventricular function impairments, and the current approaches are surgical treatment or transcatheter aortic valve replacement with prosthesis.

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“…Cardiac mitochondria use 60% to 90% of the energy originating from FA oxidation (FAO) as their primary energy source (they also use glucose, pyruvate, and lactate) to improve cardiac function, whereas most other organs use glucose as the major energy substrate [7]. Mitochondria are deeply involved in calcium (Ca 2+ ) handling [8][9][10]. Recent advances in the identification of the molecular partners regulating Ca 2+ dynamics in the mitochondrial compartment have helped elucidate the critical contributions of mitochondria to (patho) physiological conditions that rely on mitochondrial Ca 2+ oscillations [11].…”

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confidence: 99%

Mitophagy in Cardiovascular Diseases

Morciano

Patergnani

Bonora

et al. 2020

JCM

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Cardiovascular diseases are one of the leading causes of death. Increasing evidence has shown that pharmacological or genetic targeting of mitochondria can ameliorate each stage of these pathologies, which are strongly associated with mitochondrial dysfunction. Removal of inefficient and dysfunctional mitochondria through the process of mitophagy has been reported to be essential for meeting the energetic requirements and maintaining the biochemical homeostasis of cells. This process is useful for counteracting the negative phenotypic changes that occur during cardiovascular diseases, and understanding the molecular players involved might be crucial for the development of potential therapies. Here, we summarize the current knowledge on mitophagy (and autophagy) mechanisms in the context of heart disease with an important focus on atherosclerosis, ischemic heart disease, cardiomyopathies, heart failure, hypertension, arrhythmia, congenital heart disease and peripheral vascular disease. We aim to provide a complete background on the mechanisms of action of this mitochondrial quality control process in cardiology and in cardiac surgery by also reviewing studies on the use of known compounds able to modulate mitophagy for cardioprotective purposes.

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Interorganellar calcium signaling in the regulation of cell metabolism: A cancer perspective

Cited by 37 publications

References 242 publications

Caveolin-1 function at the plasma membrane and in intracellular compartments in cancer

Caveolin-1 function at the plasma membrane and in intracellular compartments in cancer

Aortic Valve Stenosis and Mitochondrial Dysfunctions: Clinical and Molecular Perspectives

Mitophagy in Cardiovascular Diseases

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