TY - JOUR
T1 - Targeting the Mitochondria-Proteostasis Axis to Delay Aging
AU - Zimmermann, Andreas
AU - Madreiter-Sokolowski, Corina
AU - Stryeck, Sarah
AU - Abdellatif, Mahmoud
N1 - Funding Information:
Funding. MA acknowledges funding received from the European Society of Cardiology in the form of an ESC Research Grant and from the Austrian Society of Cardiology (Pr?sidentenstipendium der ?KG). AZ acknowledges support from BioTechMed Graz, NAWI Graz and the Field of Excellence BioHealth at the University of Graz. CM-S was currently funded by an Erwin Schroedinger Abroad Fellowship (J4205-B27). SS was supported by H2020-JTI-EuroHPC-2019-2 (951732), Digitale und soziale Transformation in der Hochschulbildung (BMBWF, ?Austrian DataLab and Services?), and the Strategic Project Digitale TU Graz (Graz University of Technology).
Publisher Copyright:
© Copyright © 2021 Zimmermann, Madreiter-Sokolowski, Stryeck and Abdellatif.
PY - 2021/3/11
Y1 - 2021/3/11
N2 - Human life expectancy continues to grow globally, and so does the prevalence of age-related chronic diseases, causing a huge medical and economic burden on society. Effective therapeutic options for these disorders are scarce, and even if available, are typically limited to a single comorbidity in a multifaceted dysfunction that inevitably affects all organ systems. Thus, novel therapies that target fundamental processes of aging itself are desperately needed. In this article, we summarize current strategies that successfully delay aging and related diseases by targeting mitochondria and protein homeostasis. In particular, we focus on autophagy, as a fundamental proteostatic process that is intimately linked to mitochondrial quality control. We present genetic and pharmacological interventions that effectively extend health- and life-span by acting on specific mitochondrial and pro-autophagic molecular targets. In the end, we delve into the crosstalk between autophagy and mitochondria, in what we refer to as the mitochondria-proteostasis axis, and explore the prospect of targeting this crosstalk to harness maximal therapeutic potential of anti-aging interventions.
AB - Human life expectancy continues to grow globally, and so does the prevalence of age-related chronic diseases, causing a huge medical and economic burden on society. Effective therapeutic options for these disorders are scarce, and even if available, are typically limited to a single comorbidity in a multifaceted dysfunction that inevitably affects all organ systems. Thus, novel therapies that target fundamental processes of aging itself are desperately needed. In this article, we summarize current strategies that successfully delay aging and related diseases by targeting mitochondria and protein homeostasis. In particular, we focus on autophagy, as a fundamental proteostatic process that is intimately linked to mitochondrial quality control. We present genetic and pharmacological interventions that effectively extend health- and life-span by acting on specific mitochondrial and pro-autophagic molecular targets. In the end, we delve into the crosstalk between autophagy and mitochondria, in what we refer to as the mitochondria-proteostasis axis, and explore the prospect of targeting this crosstalk to harness maximal therapeutic potential of anti-aging interventions.
KW - aging
KW - anti-aging targets
KW - autophagy
KW - mitochondria
KW - proteostasis
UR - http://www.scopus.com/inward/record.url?scp=85103106070&partnerID=8YFLogxK
U2 - 10.3389/fcell.2021.656201
DO - 10.3389/fcell.2021.656201
M3 - Article
AN - SCOPUS:85103106070
SN - 2296-634X
VL - 9
JO - Frontiers in Cell and Developmental Biology
JF - Frontiers in Cell and Developmental Biology
M1 - 656201
ER -