Calorie restriction promotes cardiolipin biosynthesis and distribution between mitochondrial membranes

Luévano‐Martínez, Luis Alberto; Forni, Maria Fernanda; Peloggia, Julia; Watanabe, Ii-sei; Kowaltowski, Alicia J.

doi:10.1016/j.mad.2017.02.004

Cited by 24 publications

(13 citation statements)

References 65 publications

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“…The purity of the preparations was assessed by blotting for VDAC, an OM protein, and Cox‐III, an IM protein. The blot also shows that PLSCR3 is effectively expressed in liver mitochondria, corroborating previous studies , and that it is not found in OM preparations. We then evaluated if PLSCR3 is a true transmembrane protein by extraction in alkaline carbonate (Fig.…”

Section: Resultssupporting

confidence: 90%

Topological characterization of the mitochondrial phospholipid scramblase 3

Luévano‐Martínez

Kowaltowski

2017

FEBS Letters

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Scramblases redistribute phospholipids in biological membranes. Phospholipid scramblase 3 (PLSCR3), which is located in mitochondria, has been reported to be involved in cardiolipin distribution from the inner to the outer membrane, thus regulating cellular processes such as apoptosis or mitophagy. However, the localization and topology of this protein has not been convincingly addressed to support a role in intermembrane phospholipid transfer. Here, we studied PLSCR3 topology within mitochondria. We show that PLSCR3 inserts in the inner membrane (IM) via its C-terminal transmembrane helix, whereas its N-terminal portion is oriented toward the intermembrane space where it is activated by calcium. Our results suggest that PLSCR3, via its C-terminal transmembrane domain, participates in the bidirectional movement of phospholipids within the IM.

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Section: Resultssupporting

confidence: 90%

Topological characterization of the mitochondrial phospholipid scramblase 3

Luévano‐Martínez

Kowaltowski

2017

FEBS Letters

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“…[11][12][13][14] Increased CL at MOM has been observed under different conditions that favor mitophagy like chemical models of Parkinson disease 10 and caloric restriction. 15 Externalization of CL to the mitochondrial surface is also part of other damage-related signaling pathways, including early pro-apoptotic signaling [16][17][18] and inflammatory reactions in intracellular compartments and extracellular environments. 19 By providing a scaffold at the mitochondrial surface for recruiting and functionally altering different apoptotic proteins, including caspase 8, tBid, Bak, and Bax, [20][21][22] CL participates in launching the release of cytochrome c, [23][24][25][26][27][28] although this step may not be required for all forms of apoptosis.…”

Section: Protein and Lipid Signaling In Mitophagy And Beyondmentioning

confidence: 99%

NME4/nucleoside diphosphate kinase D in cardiolipin signaling and mitophagy

Schlattner

Tokarska‐Schlattner

Epand

et al. 2018

Laboratory Investigation

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Mitophagy is an emerging paradigm for mitochondrial quality control and cell homeostasis. Dysregulation of mitophagy can lead to human pathologies such as neurodegenerative disorders and contributes to the aging process. Complex protein signaling cascades have been described that regulate mitophagy. We have identified a novel lipid signaling pathway that involves the phospholipid cardiolipin (CL). CL is synthesized and normally confined at the inner mitochondrial membrane. However, upon a mitophagic trigger, ie, collapse of the inner membrane potential, CL is rapidly externalized to the mitochondrial surface with the assistance of the hexameric nucleoside diphosphate kinase D (NME4, NDPK-D, or NM23-H4). In addition to its NDP kinase activity, NME4/NDPK-D shows intermembrane phospholipid transfer activity in vitro and in cellular systems, which relies on NME4/NDPK-D interaction with CL, CL-dependent crosslinking of inner and outer mitochondrial membranes by symmetrical, hexameric NME4/NDPK-D, and a putative NME4/NDPK-Dbased CL-transfer pathway. CL exposed at the mitochondrial surface then serves as an 'eat me' signal for the mitophagic machinery; it is recognized by the LC3 receptor of autophagosomes, targeting the dysfunctional mitochondrion to lysosomal degradation. Similar NME4-supported CL externalization is likely also involved in apoptosis and inflammatory reactions.

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“…When studying the rate of autophagic proteolysis in the isolated livers, they found that maximum rates of autophagy were achieved in the CR groups compared to controls. A more recent study by Luevano-Martinez et al showed the effect of CR on the induction of autophagy in liver mitochondria [64]. They isolated mitochondria from the livers of controls, and after 4 months of a CR schedule, they found an increase in the LC3-II/LC3-I ratio in CR livers, indicating enhanced liver mitochondrial autophagy.…”

Section: Livermentioning

confidence: 96%

The Effects of Calorie Restriction on Autophagy: Role on Aging Intervention

Chung

2019

Nutrients

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Autophagy is an important housekeeping process that maintains a proper cellular homeostasis under normal physiologic and/or pathologic conditions. It is responsible for the disposal and recycling of metabolic macromolecules and damaged organelles through broad lysosomal degradation processes. Under stress conditions, including nutrient deficiency, autophagy is substantially activated to maintain proper cell function and promote cell survival. Altered autophagy processes have been reported in various aging studies, and a dysregulated autophagy is associated with various age-associated diseases. Calorie restriction (CR) is regarded as the gold standard for many aging intervention methods. Although it is clear that CR has diverse effects in counteracting aging process, the exact mechanisms by which it modulates those processes are still controversial. Recent advances in CR research have suggested that the activation of autophagy is linked to the observed beneficial anti-aging effects. Evidence showed that CR induced a robust autophagy response in various metabolic tissues, and that the inhibition of autophagy attenuated the anti-aging effects of CR. The mechanisms by which CR modulates the complex process of autophagy have been investigated in depth. In this review, several major advances related to CR’s anti-aging mechanisms and anti-aging mimetics will be discussed, focusing on the modification of the autophagy response.

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Calorie restriction promotes cardiolipin biosynthesis and distribution between mitochondrial membranes

Cited by 24 publications

References 65 publications

Topological characterization of the mitochondrial phospholipid scramblase 3

Topological characterization of the mitochondrial phospholipid scramblase 3

NME4/nucleoside diphosphate kinase D in cardiolipin signaling and mitophagy

The Effects of Calorie Restriction on Autophagy: Role on Aging Intervention

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