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Lipids and Mitochondria
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Lipids and Mitochondria

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (30 April 2022) | Viewed by 5531

Special Issue Editors

Dr. Sandra Merscher

E-Mail Website
Guest Editor
Department of Medicine, University of Miami Leonard M. Miller School of Medicine, Miami, FL, USA
Interests: kidney disease; mouse models; podocyte injury; diabetic kidney disease; focal segmental glomerulosclerosis; cell signaling; cholesterol; lipids; sphingolipids; TNF alpha; ABCA1; SMPDL3b
Dr. Flavia Fontanesi

E-Mail Website
Guest Editor
Department of Biochemistry & Molecular Biology, University of Miami Miller School of Medicine, Miami, FL, USA
Interests: oxidative phosphorylation; mitochondrial; assembly of mitochondrial supercomplexes; mechanisms regulating mtDNA maintenance

Special Issue Information

Dear Colleagues,

Mitochondria play a central role in cellular lipid homeostasis. On one hand, they control fatty acid catabolism; on the other, they participate in the synthesis of key membrane phospholipids.

Mitochondria provide citrate, a Krebs cycle intermediate, for lipid synthesis and housed key enzymes in the phospholipid biosynthetic pathway. Since the endoplasmic reticulum is the main site of phospholipid biosynthesis, an exchange of lipid precursors between the two organelles is required and occurs at specialized contact sites known as mitochondrial-associated membranes or MAMs. Mitochondria are also capable of synthesizing autonomously lipids such as phosphatidylglycerol and cardiolipin. The latter is a unique phospholipid located almost exclusively in the mitochondrial membranes, where it acts as a key determinant of mitochondrial morphology and dynamics. Additionally, cardiolipin regulates the biogenesis and function of inner membrane proteins, including oxidative phosphorylation enzymatic complexes.

Fatty acids are metabolized by the mitochondrion-housed pathway of fatty acid oxidation or beta-oxidation to ultimately produce cellular energy in the form of ATP molecules. Fatty acids represent the preferential substrate for ATP generation in high-energy-demanding organs such as the kidney, heart, and skeletal muscle. Moreover, the association between mitochondria and lipid droplets, the main site of triglyceride storage, is a key determinant in regulating lipid accumulation and oxidation.

This Special Issue aims to present the latest research or new views on molecular aspects of these processes, as well as on human diseases associated with dysfunctional mitochondrial lipid homeostasis. Both original research articles and comprehensive reviews are welcomed.

Dr. Sandra Merscher
Dr. Flavia Fontanesi
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • lipids
  • lipid droplets
  • mitochondria
  • lipid trafficking to mitochondria
  • fatty acid oxidation
  • beta-oxidation
  • cardiolipin (CL)
  • phosphatidylethanolamine (PE) and phosphatidylcholine (PC) biosynthesis
  • mitochondria–ER contact sites
  • mitochondria-associated membrane (MAM)
  • Barth syndrome
  • ubiquinol biosynthesis
  • mitochondria and lipid homeostasis
  • mitochondria and lipotoxicity

Published Papers (2 papers)

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Research

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18 pages, 5496 KiB  
Article
The Impact of Nicotine along with Oral Contraceptive Exposure on Brain Fatty Acid Metabolism in Female Rats
by Shahil H. Patel, Alba Timón-Gómez, Hari Pradhyumnan, Berk Mankaliye, Kunjan R. Dave, Miguel A. Perez-Pinzon and Ami P. Raval
Int. J. Mol. Sci. 2022, 23(24), 16075; https://doi.org/10.3390/ijms232416075 - 16 Dec 2022
Cited by 1 | Viewed by 1803
Abstract
Smoking-derived nicotine (N) and oral contraceptive (OC) synergistically exacerbate ischemic brain damage in females, and the underlying mechanisms remain elusive. In a previous study, we showed that N + OC exposure altered brain glucose metabolism in females. Since lipid metabolism complements glycolysis, the [...] Read more.
Smoking-derived nicotine (N) and oral contraceptive (OC) synergistically exacerbate ischemic brain damage in females, and the underlying mechanisms remain elusive. In a previous study, we showed that N + OC exposure altered brain glucose metabolism in females. Since lipid metabolism complements glycolysis, the current study aims to examine the metabolic fingerprint of fatty acids in the brain of female rats exposed to N+/−OC. Adolescent and adult Sprague–Dawley female rats were randomly (n = 8 per group) exposed to either saline or N (4.5 mg/kg) +/−OC (combined OC or placebo delivered via oral gavage) for 16–21 days. Following exposure, brain tissue was harvested for unbiased metabolomic analysis (performed by Metabolon Inc., Morrisville, NC, USA) and the metabolomic profile changes were complemented with Western blot analysis of key enzymes in the lipid pathway. Metabolomic data showed significant accumulation of fatty acids and phosphatidylcholine (PC) metabolites in the brain. Adolescent, more so than adult females, exposed to N + OC showed significant increases in carnitine-conjugated fatty acid metabolites compared to saline control animals. These changes in fatty acyl carnitines were accompanied by an increase in a subset of free fatty acids, suggesting elevated fatty acid β-oxidation in the mitochondria to meet energy demand. In support, β-hydroxybutyrate was significantly lower in N + OC exposure groups in adolescent animals, implying a complete shunting of acetyl CoA for energy production via the TCA cycle. The reported changes in fatty acids and PC metabolism due to N + OC could inhibit post-translational palmitoylation of membrane proteins and synaptic vesicle formation, respectively, thus exacerbating ischemic brain damage in female rats. Full article
(This article belongs to the Special Issue Lipids and Mitochondria)
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Review

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17 pages, 2561 KiB  
Review
Crosstalk between Mitochondrial Protein Import and Lipids
by Juliane J. Hoffmann and Thomas Becker
Int. J. Mol. Sci. 2022, 23(9), 5274; https://doi.org/10.3390/ijms23095274 - 09 May 2022
Cited by 7 | Viewed by 3080
Abstract
Mitochondria import about 1000 precursor proteins from the cytosol. The translocase of the outer membrane (TOM complex) forms the major entry site for precursor proteins. Subsequently, membrane-bound protein translocases sort the precursor proteins into the outer and inner membrane, the intermembrane space, and [...] Read more.
Mitochondria import about 1000 precursor proteins from the cytosol. The translocase of the outer membrane (TOM complex) forms the major entry site for precursor proteins. Subsequently, membrane-bound protein translocases sort the precursor proteins into the outer and inner membrane, the intermembrane space, and the matrix. The phospholipid composition of mitochondrial membranes is critical for protein import. Structural and biochemical data revealed that phospholipids affect the stability and activity of mitochondrial protein translocases. Integration of proteins into the target membrane involves rearrangement of phospholipids and distortion of the lipid bilayer. Phospholipids are present in the interface between subunits of protein translocases and affect the dynamic coupling of partner proteins. Phospholipids are required for full activity of the respiratory chain to generate membrane potential, which in turn drives protein import across and into the inner membrane. Finally, outer membrane protein translocases are closely linked to organellar contact sites that mediate lipid trafficking. Altogether, intensive crosstalk between mitochondrial protein import and lipid biogenesis controls mitochondrial biogenesis. Full article
(This article belongs to the Special Issue Lipids and Mitochondria)
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