Mitochondrial calcium signalling and neurodegenerative diseases

Britti, Elena; Delaspre, Fabien; Tamarit, Jordi; Ros, Joaquim

doi:10.1042/ns20180061

Cited by 34 publications

(21 citation statements)

References 132 publications

(149 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Release and re-uptake of Ca 2+ to/from the cytosol mediate initiation and termination of many cellular responses to signals. ER is a major calcium store and manages Ca 2+ homeostasis by either behaving as a local Ca 2+ sink, or a store that releases Ca 2+ to other cellular compartments (Raffaello et al, 2016), controlling processes such as mitochondrial homeostasis and function (Britti et al, 2018). ER can buffer excess presynaptic cytosolic Ca 2+ during repetitive firing, by uptake via the SERCA calcium ATPase (Sanyal et al, 2005) or potentially also the SPoCk ATPase (Southall et al, 2006).…”

Section: Protein Function Axonal Localizationmentioning

confidence: 99%

Axonal Endoplasmic Reticulum Dynamics and Its Roles in Neurodegeneration

2020

View full text Add to dashboard Cite

The physical continuity of axons over long cellular distances poses challenges for their maintenance. One organelle that faces this challenge is endoplasmic reticulum (ER); unlike other intracellular organelles, this forms a physically continuous network throughout the cell, with a single membrane and a single lumen. In axons, ER is mainly smooth, forming a tubular network with occasional sheets or cisternae and low amounts of rough ER. It has many potential roles: lipid biosynthesis, glucose homeostasis, a Ca 2+ store, protein export, and contacting and regulating other organelles. This tubular network structure is determined by ER-shaping proteins, mutations in some of which are causative for neurodegenerative disorders such as hereditary spastic paraplegia (HSP). While axonal ER shares many features with the tubular ER network in other contexts, these features must be adapted to the long and narrow dimensions of axons. ER appears to be physically continuous throughout axons, over distances that are enormous on a subcellular scale. It is therefore a potential channel for long-distance or regional communication within neurons, independent of action potentials or physical transport of cargos, but involving its physiological roles such as Ca 2+ or organelle homeostasis. Despite its apparent stability, axonal ER is highly dynamic, showing features like anterograde and retrograde transport, potentially reflecting continuous fusion and breakage of the network. Here we discuss the transport processes that must contribute to this dynamic behavior of ER. We also discuss the model that these processes underpin a homeostatic process that ensures both enough ER to maintain continuity of the network and repair breaks in it, but not too much ER that might disrupt local cellular physiology. Finally, we discuss how failure of ER organization in axons could lead to axon degenerative diseases, and how a requirement for ER continuity could make distal axons most susceptible to degeneration in conditions that disrupt ER continuity.

show abstract

Section: Protein Function Axonal Localizationmentioning

confidence: 99%

Axonal Endoplasmic Reticulum Dynamics and Its Roles in Neurodegeneration

2020

View full text Add to dashboard Cite

show abstract

“…mPTP/mPTPC (mitochondrial permeability transition pore or mPTP complex): mPTP or mPTPC is considered as the main transport system for Ca 2+ efflux from mitochondria under pathophysiological conditions [ 2 , 3 , 12 , 31 , 32 , 128 , 129 , 130 , 131 , 132 , 133 , 134 ]. Although the mPTPC was initially described in swelling experiments using the fraction of isolated mitochondria and characterized as a non-selective channel that transports ionic and nonionic molecules as early as 1979 [ 110 ], the transport mechanism of this channel actually remains poorly understood.…”

Section: Calcium Transport Systems In Mitochondriamentioning

confidence: 99%

Regulation of Cell Death by Mitochondrial Transport Systems of Calcium and Bcl-2 Proteins

Naumova

Šachl

2020

Membranes

View full text Add to dashboard Cite

Mitochondria represent the fundamental system for cellular energy metabolism, by not only supplying energy in the form of ATP, but also by affecting physiology and cell death via the regulation of calcium homeostasis and the activity of Bcl-2 proteins. A lot of research has recently been devoted to understanding the interplay between Bcl-2 proteins, the regulation of these interactions within the cell, and how these interactions lead to the changes in calcium homeostasis. However, the role of Bcl-2 proteins in the mediation of mitochondrial calcium homeostasis, and therefore the induction of cell death pathways, remain underestimated and are still not well understood. In this review, we first summarize our knowledge about calcium transport systems in mitochondria, which, when miss-regulated, can induce necrosis. We continue by reviewing and analyzing the functions of Bcl-2 proteins in apoptosis. Finally, we link these two regulatory mechanisms together, exploring the interactions between the mitochondrial Ca2+ transport systems and Bcl-2 proteins, both capable of inducing cell death, with the potential to determine the cell death pathway—either the apoptotic or the necrotic one.

show abstract

“…Mitochondria are no longer static organs as ATP producers, but also as a store of various lethal proteins which will be released in programmed cell death and this is an important intracellular calcium signal. Since the expression of the calcium transport membrane in the mitochondria has been found, the process of signaling calcium in the mitochondria has become clear [34][35][36] Calcium is inserted into the membrane in the mitochondria by the uniporter. Uniporter activity is influenced by temperature and cation selectivity so that it can almost be called a channel rather than a career.…”

Section: Mitochondria and Calcium Signalingmentioning

confidence: 99%

Calcium Dyshomeostasis in Neuropathy Diabetes

Kurniawan¹

2020

Weight Management

View full text Add to dashboard Cite

Diabetes is a ceaseless ailment that is basic in practically all nations. Neuropathy is the most well-known constant difficulty of diabetes and is the underlying reason for ulceration in the legs of lower appendage removals. The predominance of diabetic polyneuropathy shifts from 23 to 29%. Incessant metabolic pressure incited by hyperglycemia, either low insulin creation in type 1 diabetes or diminished fringe affectability to insulin in type 2 diabetes influences cell homeostasis in practically all phone types. Changes in the sign Ca 2+ have been recognized in different seclusion tissues from creatures initiated to diabetes just as patients with diabetes. Ca 2+ homeostasis variations from the norm have likewise been found in an assortment of tissues, including bone, heart and smooth muscle, secretory cells, platelets, kidneys and osteoblasts. This variation from the norm by and large shows as an expanded resting centralization of intracellular Ca 2+ ([Ca 2+ ]I), diminished Ca 2+ transporter movement and diminished boost that produces Ca 2+ signals. Ca 2+ flagging issue are likewise found in neuron-sensory from trial creatures with diabetes.

show abstract

Mitochondrial calcium signalling and neurodegenerative diseases

Cited by 34 publications

References 132 publications

Axonal Endoplasmic Reticulum Dynamics and Its Roles in Neurodegeneration

Axonal Endoplasmic Reticulum Dynamics and Its Roles in Neurodegeneration

Regulation of Cell Death by Mitochondrial Transport Systems of Calcium and Bcl-2 Proteins

Calcium Dyshomeostasis in Neuropathy Diabetes

Contact Info

Product

Resources

About