Restoring calcium crosstalk between ER and mitochondria promotes intestinal stem cell rejuvenation through autophagy in aged Drosophila

Abstract Breakdown of calcium network is closely associated with cellular aging. Previously, we found that cytosolic calcium (CytoCa2+) levels were elevated while mitochondrial calcium (MitoCa2+) levels were decreased and associated with metabolic shift in aged intestinal stem cells (ISCs) of Drosop...

Full description

Saved in:
Bibliographic Details
Main Authors: Yao Zhang, Peng Ma, Saifei Wang, Shuxin Chen, Hansong Deng
Format: Article
Language:English
Published: Nature Portfolio 2025-05-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-025-60196-4
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850231377084022784
author Yao Zhang
Peng Ma
Saifei Wang
Shuxin Chen
Hansong Deng
author_facet Yao Zhang
Peng Ma
Saifei Wang
Shuxin Chen
Hansong Deng
author_sort Yao Zhang
collection DOAJ
description Abstract Breakdown of calcium network is closely associated with cellular aging. Previously, we found that cytosolic calcium (CytoCa2+) levels were elevated while mitochondrial calcium (MitoCa2+) levels were decreased and associated with metabolic shift in aged intestinal stem cells (ISCs) of Drosophila. How MitoCa2+ was decoupled from the intracellular calcium network and whether the reduction of MitoCa2+ drives ISC aging, however, remains unresolved. Here, we show that genetically restoring MitoCa2+ can reverse ISC functional decline and promote intestinal homeostasis by activating autophagy in aged flies. Further studies indicate that MitoCa2+ and Mitochondria–ER contacts (MERCs) form a positive feedback loop via IP3R to regulate autophagy independent of AMPK. Breakdown of this loop is responsible for MitoCa2+ reduction and ISC dysfunction in aged flies. Our results identify a regulatory module for autophagy initiation involving calcium crosstalk between the ER and mitochondria, providing a strategy to treat aging and age-related diseases.
format Article
id doaj-art-b4d67420dd914a7ebbd5176c1c87f24d
institution OA Journals
issn 2041-1723
language English
publishDate 2025-05-01
publisher Nature Portfolio
record_format Article
series Nature Communications
spelling doaj-art-b4d67420dd914a7ebbd5176c1c87f24d2025-08-20T02:03:32ZengNature PortfolioNature Communications2041-17232025-05-0116111710.1038/s41467-025-60196-4Restoring calcium crosstalk between ER and mitochondria promotes intestinal stem cell rejuvenation through autophagy in aged DrosophilaYao Zhang0Peng Ma1Saifei Wang2Shuxin Chen3Hansong Deng4Yangzhi Rehabilitation Hospital, Sunshine Rehabilitation Center, Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji UniversityYangzhi Rehabilitation Hospital, Sunshine Rehabilitation Center, Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji UniversityYangzhi Rehabilitation Hospital, Sunshine Rehabilitation Center, Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji UniversityYangzhi Rehabilitation Hospital, Sunshine Rehabilitation Center, Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji UniversityYangzhi Rehabilitation Hospital, Sunshine Rehabilitation Center, Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji UniversityAbstract Breakdown of calcium network is closely associated with cellular aging. Previously, we found that cytosolic calcium (CytoCa2+) levels were elevated while mitochondrial calcium (MitoCa2+) levels were decreased and associated with metabolic shift in aged intestinal stem cells (ISCs) of Drosophila. How MitoCa2+ was decoupled from the intracellular calcium network and whether the reduction of MitoCa2+ drives ISC aging, however, remains unresolved. Here, we show that genetically restoring MitoCa2+ can reverse ISC functional decline and promote intestinal homeostasis by activating autophagy in aged flies. Further studies indicate that MitoCa2+ and Mitochondria–ER contacts (MERCs) form a positive feedback loop via IP3R to regulate autophagy independent of AMPK. Breakdown of this loop is responsible for MitoCa2+ reduction and ISC dysfunction in aged flies. Our results identify a regulatory module for autophagy initiation involving calcium crosstalk between the ER and mitochondria, providing a strategy to treat aging and age-related diseases.https://doi.org/10.1038/s41467-025-60196-4
spellingShingle Yao Zhang
Peng Ma
Saifei Wang
Shuxin Chen
Hansong Deng
Restoring calcium crosstalk between ER and mitochondria promotes intestinal stem cell rejuvenation through autophagy in aged Drosophila
Nature Communications
title Restoring calcium crosstalk between ER and mitochondria promotes intestinal stem cell rejuvenation through autophagy in aged Drosophila
title_full Restoring calcium crosstalk between ER and mitochondria promotes intestinal stem cell rejuvenation through autophagy in aged Drosophila
title_fullStr Restoring calcium crosstalk between ER and mitochondria promotes intestinal stem cell rejuvenation through autophagy in aged Drosophila
title_full_unstemmed Restoring calcium crosstalk between ER and mitochondria promotes intestinal stem cell rejuvenation through autophagy in aged Drosophila
title_short Restoring calcium crosstalk between ER and mitochondria promotes intestinal stem cell rejuvenation through autophagy in aged Drosophila
title_sort restoring calcium crosstalk between er and mitochondria promotes intestinal stem cell rejuvenation through autophagy in aged drosophila
url https://doi.org/10.1038/s41467-025-60196-4
work_keys_str_mv AT yaozhang restoringcalciumcrosstalkbetweenerandmitochondriapromotesintestinalstemcellrejuvenationthroughautophagyinageddrosophila
AT pengma restoringcalciumcrosstalkbetweenerandmitochondriapromotesintestinalstemcellrejuvenationthroughautophagyinageddrosophila
AT saifeiwang restoringcalciumcrosstalkbetweenerandmitochondriapromotesintestinalstemcellrejuvenationthroughautophagyinageddrosophila
AT shuxinchen restoringcalciumcrosstalkbetweenerandmitochondriapromotesintestinalstemcellrejuvenationthroughautophagyinageddrosophila
AT hansongdeng restoringcalciumcrosstalkbetweenerandmitochondriapromotesintestinalstemcellrejuvenationthroughautophagyinageddrosophila