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:	Mechanisms by which PE21, an extract from the white willow Salix alba, delays chronological aging in budding yeast.
Authors:	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
Link:	https://www.ncbi.nlm.nih.gov/pubmed/31645900?dopt=Abstract
DOI:	10.18632/oncotarget.27209
Publication:	Oncotarget
Keywords:	cellular aging; geroprotectors; lipid metabolism; mitochondria; necrotic cell death;
PMID:	31645900	Category:	Oncotarget	Date Added:	2019-10-25
Dept Affiliation:	BIOLOGY 1 Department of Biology, Concordia University, Montreal, Quebec H4B 1R6, Canada. 2 Idunn Technologies Inc., Rosemere, Quebec J7A 4A5, Canada.

Description:

Mechanisms by which PE21, an extract from the white willow Salix alba, delays chronological aging in budding yeast.

Oncotarget. 2019 Oct 08;10(56):5780-5816

Authors: 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

Abstract

We have recently found that PE21, an extract from the white willow Salix alba, slows chronological aging and prolongs longevity of the yeast Saccharomyces cerevisiae more efficiently than any of the previously known pharmacological interventions. Here, we investigated mechanisms through which PE21 delays yeast chronological aging and extends yeast longevity. We show that PE21 causes a remodeling of lipid metabolism in chronologically aging yeast, thereby instigating changes in the concentrations of several lipid classes. We demonstrate that such changes in the cellular lipidome initiate three mechanisms of aging delay and longevity extension. The first mechanism through which PE21 slows aging and prolongs longevity consists in its ability to decrease the intracellular concentration of free fatty acids. This postpones an age-related onset of liponecrotic cell death promoted by excessive concentrations of free fatty acids. The second mechanism of aging delay and longevity extension by PE21 consists in its ability to decrease the concentrations of triacylglycerols and to increase the concentrations of glycerophospholipids within the endoplasmic reticulum membrane. This activates the unfolded protein response system in the endoplasmic reticulum, which then decelerates an age-related decline in protein and lipid homeostasis and slows down an aging-associated deterioration of cell resistance to stress. The third mechanisms underlying aging delay and longevity extension by PE21 consists in its ability to change lipid concentrations in the mitochondrial membranes. This alters certain catabolic and anabolic processes in mitochondria, thus amending the pattern of aging-associated changes in several key aspects of mitochondrial functionality.

PMID: 31645900 [PubMed]

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