TY  - JOUR
AB  - Calcium (Ca2+) signalling acts a pleiotropic message within the cell that is decoded by the mitochondria through a sophisticated ion channel known as the Mitochondrial Ca2+ Uniporter (MCU) complex. Under physiological conditions, mitochondrial Ca2+ signalling is crucial for coordinating cell activation with energy production. Conversely, in pathological scenarios, it can determine the fine balance between cell survival and death. Over the last decade, significant progress has been made in understanding the molecular bases of mitochondrial Ca2+ signalling. This began with the elucidation of the MCU channel components and extended to the elucidation of the mechanisms that regulate its activity. Additionally, increasing evidence suggests molecular mechanisms allowing tissue-specific modulation of the MCU complex, tailoring channel activity to the specific needs of different tissues or cell types. This review aims to explore the latest evidence elucidating the regulation of the MCU complex, the molecular factors controlling the tissue-specific properties of the channel, and the physiological and pathological implications of mitochondrial Ca2+ signalling in different tissues.
AU  - Vecellio Reane, D.
AU  - Serna, J.D.C.*
AU  - Raffaello, A.*
C1  - 70766
C2  - 55737
CY  - 125 London Wall, London, England
TI  - Unravelling the complexity of the mitochondrial Ca2+ uniporter: Regulation, tissue specificity, and physiological implications.
JO  - Cell Calcium
VL  - 121
PB  - Elsevier Sci Ltd
PY  - 2024
SN  - 0143-4160
ER  - 

TY  - JOUR
AB  - Ferroptosis is an iron-dependent form of cell death triggered by dysregulation of biochemical processes that culminate in lethal lipid peroxidation. Lipid metabolism is fundamental for determining ferroptotic fate, however, the mechanisms that alter lipid components to shape ferroptosis susceptibility remains elusive. A recent article by Lin and colleagues in Nature Communications systematically analyzed phospholipid transporters (phospholipid scramblases, flippases, and floppases), and identified that the lipid flippase solute carrier family 47 member 1 (SLC47A1) functions as a regulator of lipid remodeling and promotes ferroptosis resistance. SLC47A1 is transactivated by peroxisome proliferator activated receptor alpha (PPARA). Upon ferroptosis induction, SLC47A1 upregulation inhibits DHA/DPA polyunsaturated fatty acid containing glycerophospholipids (PUFA-PLs) accumulation to block ferroptosis. Depletion of either PPARA or SLC47A1 sensitized cells to ferroptosis by favoring ACSL4-SOAT1–mediated production of polyunsaturated fatty acid containing (PUFA) cholesterol esters. Ferroptosis has been widely linked to degenerative processes and tumor suppression. These findings indicate that lipid transporters may provide yet another means by which PUFA-containing membrane lipids convey ferroptosis sensitivity.
AU  - Xin, S.
AU  - Schick, J.A.
C1  - 67435
C2  - 54136
CY  - The Boulevard, Langford Lane, Kidlington, Oxford Ox5 1gb, Oxon, England
TI  - PUFAs dictate the balance of power in ferroptosis.
JO  - Cell Calcium
VL  - 110
PB  - Elsevier Sci Ltd
PY  - 2023
SN  - 0143-4160
ER  - 

TY  - JOUR
AB  - Human mitochondria are complex and highly dynamic biological systems, comprised of over a thousand parts and evolved to fully integrate into the specialized intracellular signaling networks and metabolic requirements of each cell and organ. Over the last two decades, several complementary, top-down computational and experimental approaches have been developed to identify, characterize and modulate the human mitochondrial system, demonstrating the power of integrating classical reductionist and discovery-driven analyses in order to de-orphanize hitherto unknown molecular components of mitochondrial machineries and pathways. To this goal, systematic, multiomics-based surveys of proteome composition, protein networks, and phenotype-to-pathway associations at the tissue, cell and organellar level have been largely exploited to predict the full complement of mitochondrial proteins and their functional interactions, therefore catalyzing data-driven hypotheses. Collectively, these multidisciplinary and integrative research approaches hold the potential to propel our understanding of mitochondrial biology and provide a systems-level framework to unraveling mitochondria-mediated and disease-spanning pathomechanisms.
AU  - Delgado De La Herran, H.C.
AU  - Cheng, Y.
AU  - Perocchi, F.
C1  - 61378
C2  - 50182
CY  - The Boulevard, Langford Lane, Kidlington, Oxford Ox5 1gb, Oxon, England
TI  - Towards a systems-level understanding of mitochondrial biology.
JO  - Cell Calcium
VL  - 95
PB  - Elsevier Sci Ltd
PY  - 2021
SN  - 0143-4160
ER  - 

TY  - JOUR
AB  - Extra and intracellular magnesium is involved in the control of myocardial calcium movements. Here we report on an increase in cytosolic calcium concentration in resting ventricular myocytes due to the withdrawal of extracellular magnesium under the condition of a blocked sodium-dependent calcium elimination. Evidence for an activation of cellular calcium efflux by extracellular magnesium showed experiments in perfused hearts. It is concluded that extracellular magnesium can modulate the intracellular free calcium concentration of the myocardial cell by its influence on calcium elimination.
AU  - Vierling, W.*
AU  - Stampfl, A.
C1  - 40026
C2  - 38050
SP  - 175-182
TI  - Magnesium-dependent calcium efflux in mammalian heart muscle.
JO  - Cell Calcium
VL  - 15
IS  - 2
PY  - 1994
SN  - 0143-4160
ER  -