PERFORM Publications

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Title		Authors	PubMed ID
1	The effect of 14 days Actovegin administration with or without high intensity training on exercise capacity and skeletal muscle mitochondrial respiration	Hassø RK; Lindtofte S; Kosik B; Bergdahl A; Larsen S;	41553522 HKAP
2	Cross-species evaluation of TANGO2 homologs, including HRG-9 and HRG-10 in em Caenorhabditis elegans, /em challenges a proposed role in heme trafficking	Sandkuhler SE; Youngs KS; Gottipalli O; Owlett LD; Bandora MB; Naaz A; Kim E; Wang L; Wojtovich A; Gupta V; Sacher M; Mackenzie SJ;	41504601 BIOLOGY
3	Reduced 17β-estradiol following ovariectomy induces mitochondrial dysfunction and degradation of synaptic proteins in the entorhinal cortex	Olajide OJ; Batallán Burrowes AA; da Silva IF; Bergdahl A; Chapman CA;	39617168 HKAP
4	A polyphenol-rich cranberry supplement improves muscle oxidative capacity in healthy adults	Parenteau F; Denis A; Roberts M; Comtois AS; Bergdahl A;	38626462 HKAP
5	Actovegin improves skeletal muscle mitochondrial respiration and functional aerobic capacity in a type 1 diabetic male murine model	Kosik B; Larsen S; Bergdahl A;	37913525 HKAP
6	Physiological levels of cardiolipin acutely affect mitochondrial respiration in vascular smooth muscle cells	Galambo D; Bergdahl A;	36594049 HKAP
7	Inhibiting amyloid beta (1-42) peptide-induced mitochondrial dysfunction prevents the degradation of synaptic proteins in the entorhinal cortex	Olajide OJ; La Rue C; Bergdahl A; Chapman CA;	36275011 HKAP
8	Characterization of Affective Behaviors and Motor Functions in Mice With a Striatal-Specific Deletion of Bmal1 and Per2	Schoettner K; Alonso M; Button M; Goldfarb C; Herrera J; Quteishat N; Meyer C; Bergdahl A; Amir S;	35755440 HKAP
9	The phenotype associated with variants in TANGO2 may be explained by a dual role of the protein in ER-to-Golgi transport and at the mitochondria.	Milev MP, Saint-Dic D, Zardoui K, Klopstock T, Law C, Distelmaier F, Sacher M	32909282 BIOLOGY
10	Mechanisms by which PE21, an extract from the white willow Salix alba, delays chronological aging in budding yeast.	Medkour Y, Mohammad K, Arlia-Ciommo A, Svistkova V, Dakik P, Mitrofanova D, Rodriguez MEL, Junio JAB, Taifour T, Escudero P, Goltsios FF, Soodbakhsh S, Maalaoui H, Simard É, Titorenko VI	31645900 BIOLOGY
11	Lithocholic bile acid accumulated in yeast mitochondria orchestrates a development of an anti-aging cellular pattern by causing age-related changes in cellular proteome.	Beach A, Richard VR, Bourque S, Boukh-Viner T, Kyryakov P, Gomez-Perez A, Arlia-Ciommo A, Feldman R, Leonov A, Piano A, Svistkova V, Titorenko VI	25839782 MASSSPEC
12	Some Metabolites Act as Second Messengers in Yeast Chronological Aging.	Mohammad K, Dakik P, Medkour Y, McAuley M, Mitrofanova D, Titorenko VI	29543708 BIOLOGY
13	Caloric restriction delays yeast chronological aging by remodeling carbohydrate and lipid metabolism, altering peroxisomal and mitochondrial functionalities, and postponing the onsets of apoptotic and liponecrotic modes of regulated cell death.	Arlia-Ciommo A, Leonov A, Beach A, Richard VR, Bourque SD, Burstein MT, Kyryakov P, Gomez-Perez A, Koupaki O, Feldman R, Titorenko VI	29662634 BIOLOGY

Title:	Caloric restriction delays yeast chronological aging by remodeling carbohydrate and lipid metabolism, altering peroxisomal and mitochondrial functionalities, and postponing the onsets of apoptotic and liponecrotic modes of regulated cell death.
Authors:	Arlia-Ciommo A, Leonov A, Beach A, Richard VR, Bourque SD, Burstein MT, Kyryakov P, Gomez-Perez A, Koupaki O, Feldman R, Titorenko VI
Link:	https://www.ncbi.nlm.nih.gov/pubmed/29662634?dopt=Abstract
DOI:	10.18632/oncotarget.24604
Publication:	Oncotarget
Keywords:	caloric restriction; cellular aging; metabolism; mitochondria; yeast;
PMID:	29662634	Category:	Oncotarget	Date Added:	2019-06-07
Dept Affiliation:	BIOLOGY 1 Department of Biology, Concordia University, Montreal, Quebec, Canada.

Description:

Caloric restriction delays yeast chronological aging by remodeling carbohydrate and lipid metabolism, altering peroxisomal and mitochondrial functionalities, and postponing the onsets of apoptotic and liponecrotic modes of regulated cell death.

Oncotarget. 2018 Mar 23;9(22):16163-16184

Authors: Arlia-Ciommo A, Leonov A, Beach A, Richard VR, Bourque SD, Burstein MT, Kyryakov P, Gomez-Perez A, Koupaki O, Feldman R, Titorenko VI

Abstract

A dietary regimen of caloric restriction delays aging in evolutionarily distant eukaryotes, including the budding yeast Saccharomyces cerevisiae. Here, we assessed how caloric restriction influences morphological, biochemical and cell biological properties of chronologically aging yeast advancing through different stages of the aging process. Our findings revealed that this low-calorie diet slows yeast chronological aging by mechanisms that coordinate the spatiotemporal dynamics of various cellular processes before entry into a non-proliferative state and after such entry. Caloric restriction causes a stepwise establishment of an aging-delaying cellular pattern by tuning a network that assimilates the following: 1) pathways of carbohydrate and lipid metabolism; 2) communications between the endoplasmic reticulum, lipid droplets, peroxisomes, mitochondria and the cytosol; and 3) a balance between the processes of mitochondrial fusion and fission. Through different phases of the aging process, the caloric restriction-dependent remodeling of this intricate network 1) postpones the age-related onsets of apoptotic and liponecrotic modes of regulated cell death; and 2) actively increases the chance of cell survival by supporting the maintenance of cellular proteostasis. Because caloric restriction decreases the risk of cell death and actively increases the chance of cell survival throughout chronological lifespan, this dietary intervention extends longevity of chronologically aging yeast.

PMID: 29662634 [PubMed]

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