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Mechanisms that Link Chronological Aging to Cellular Quiescence in Budding Yeast.

Author(s): Mohammad K, Baratang Junio JA, Tafakori T, Orfanos E, Titorenko VI

Int J Mol Sci. 2020 Jul 02;21(13): Authors: Mohammad K, Baratang Junio JA, Tafakori T, Orfanos E, Titorenko VI

Article GUID: 32630624
Mechanisms by which PE21, an extract from the white willow Salix alba, delays chronological aging in budding yeast.

Author(s): Medkour Y, Mohammad K, Arlia-Ciommo A, Svistkova V, Dakik P, Mitrofanova D, Rodriguez MEL, Junio JAB, Taifour T, Escudero P, Goltsios FF, So...

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, Soodbakh...

Article GUID: 31645900
Lipid metabolism and transport define longevity of the yeast Saccharomyces cerevisiae.

Author(s): Mitrofanova D, Dakik P, McAuley M, Medkour Y, Mohammad K, Titorenko VI

Front Biosci (Landmark Ed). 2018 Jan 01;23:1166-1194 Authors: Mitrofanova D, Dakik P, McAuley M, Medkour Y, Mohammad K, Titorenko VI

Article GUID: 28930594
Some Metabolites Act as Second Messengers in Yeast Chronological Aging.

Author(s): Mohammad K, Dakik P, Medkour Y, McAuley M, Mitrofanova D, Titorenko VI

Int J Mol Sci. 2018 Mar 15;19(3): Authors: Mohammad K, Dakik P, Medkour Y, McAuley M, Mitrofanova D, Titorenko VI

Article GUID: 29543708
Yeast Cells Exposed to Exogenous Palmitoleic Acid Either Adapt to Stress and Survive or Commit to Regulated Liponecrosis and Die.

Author(s): Mohammad K, Dakik P, Medkour Y, McAuley M, Mitrofanova D, Titorenko VI

Oxid Med Cell Longev. 2018;2018:3074769 Authors: Mohammad K, Dakik P, Medkour Y, McAuley M, Mitrofanova D, Titorenko VI

Article GUID: 29636840
Yeast chronological aging is linked to cell cycle regulation.

Author(s): Mohammad K, Titorenko VI

Cell Cycle. 2018;17(9):1035-1036 Authors: Mohammad K, Titorenko VI PMID: 29895227 [PubMed - in process]

Article GUID: 29895227
Mechanisms through which lithocholic acid delays yeast chronological aging under caloric restriction conditions.

Author(s): Arlia-Ciommo A, Leonov A, Mohammad K, Beach A, Richard VR, Bourque SD, Burstein MT, Goldberg AA, Kyryakov P, Gomez-Perez A, Koupaki O, Titorenko VI

Oncotarget. 2018 Oct 09;9(79):34945-34971 Authors: Arlia-Ciommo A, Leonov A, Mohammad K, Beach A, Richard VR, Bourque SD, Burstein MT, Goldberg AA, Kyryakov P, Gomez-Perez A, Koupaki O, Titorenko VI

Article GUID: 30405886
Quiescence Entry, Maintenance, and Exit in Adult Stem Cells.

Author(s): Mohammad K, Dakik P, Medkour Y, Mitrofanova D, Titorenko VI

Int J Mol Sci. 2019 May 01;20(9): Authors: Mohammad K, Dakik P, Medkour Y, Mitrofanova D, Titorenko VI

Article GUID: 31052375
Mechanisms Through Which Some Mitochondria-Generated Metabolites Act as Second Messengers That Are Essential Contributors to the Aging Process in Eukaryotes Across Phyla.

Author(s): Dakik P, Medkour Y, Mohammad K, Titorenko VI

Front Physiol. 2019;10:461 Authors: Dakik P, Medkour Y, Mohammad K, Titorenko VI

Article GUID: 31057428
Title:Mechanisms Through Which Some Mitochondria-Generated Metabolites Act as Second Messengers That Are Essential Contributors to the Aging Process in Eukaryotes Across Phyla.
Authors:Dakik P,  Medkour Y,  Mohammad K,  Titorenko VI
Link:https://www.ncbi.nlm.nih.gov/pubmed/31057428?dopt=Abstract
Category:Front Physiol
PMID:31057428
Dept Affiliation: BIOLOGY
1 Department of Biology, Concordia University, Montreal, QC, Canada.

Description:

Mechanisms Through Which Some Mitochondria-Generated Metabolites Act as Second Messengers That Are Essential Contributors to the Aging Process in Eukaryotes Across Phyla.

Front Physiol. 2019;10:461

Authors: Dakik P, Medkour Y, Mohammad K, Titorenko VI

Abstract

Recent studies have revealed that some low-molecular weight molecules produced in mitochondria are essential contributing factors to aging and aging-associated pathologies in evolutionarily distant eukaryotes. These molecules are intermediates or products of certain metabolic reactions that are activated in mitochondria in response to specific changes in the nutrient, stress, proliferation, or age status of the cell. After being released from mitochondria, these metabolites directly or indirectly change activities of a distinct set of protein sensors that reside in various cellular locations outside of mitochondria. Because these protein sensors control the efficiencies of some pro- or anti-aging cellular processes, such changes in their activities allow to create a pro- or anti-aging cellular pattern. Thus, mitochondria can function as signaling platforms that respond to certain changes in cell stress and physiology by remodeling their metabolism and releasing a specific set of metabolites known as "mitobolites." These mitobolites then define the pace of cellular and organismal aging because they regulate some longevity-defining processes taking place outside of mitochondria. In this review, we discuss recent progress in understanding mechanisms underlying the ability of mitochondria to function as such signaling platforms in aging and aging-associated diseases.

PMID: 31057428 [PubMed]