REDD1 attenuates cardiac hypertrophy via enhancing autophagy

Liu, Chen; Xue, Rui‐De; Wu, Dexi; Wu, Lingling; Chen, Cong; Tan, Weiping; Chen, Yili; Dong, Yugang

doi:10.1016/j.bbrc.2014.10.079

Cited by 34 publications

(26 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We report that a number of CEN-specific SDEGs are from the longevity-associated pathways, such as mTOR, insulin/ IGF-1, and p53 (Supplemental Table S6; Lin et al 2001;Tavernarakis et al 2008;Johnson et al 2013); several of these genes are located in the nodes of the pathways and consistently have the potential to induce autophagy. For example, the decreased expression of IGF1R and IRS1 genes can activate autophagic function via decreasing insulin/IGF-1 signal (Rubinsztein et al 2011), while the higher expression of the DDIT4 gene could promote autophagy through suppressing the mTOR signaling pathway (Liu et al 2014). These findings underscore a crucial role for autophagy in human longevity.…”

Section: Discussionmentioning

confidence: 87%

Transcriptome evidence reveals enhanced autophagy-lysosomal function in centenarians

Xiao

Chen

et al. 2018

Genome Res.

View full text Add to dashboard Cite

Centenarians (CENs) are excellent subjects to study the mechanisms of human longevity and healthy aging. Here, we analyzed the transcriptomes of 76 centenarians, 54 centenarian-children, and 41 spouses of centenarian-children by RNA sequencing and found that, among the significantly differentially expressed genes (SDEGs) exhibited by CENs, the autophagy-lysosomal pathway is significantly up-regulated. Overexpression of several genes from this pathway, CTSB, ATP6V0C, ATG4D, and WIPI1, could promote autophagy and delay senescence in cultured IMR-90 cells, while overexpression of the Drosophila homolog of WIPI1, Atg18a, extended the life span in transgenic flies. Interestingly, the enhanced autophagylysosomal activity could be partially passed on to their offspring, as manifested by their higher levels of both autophagyencoding genes and serum beclin 1 (BECN1). In light of the normal age-related decline of autophagy-lysosomal functions, these findings provide a compelling explanation for achieving longevity in, at least, female CENs, given the gender bias in our collected samples, and suggest that the enhanced waste-cleaning activity via autophagy may serve as a conserved mechanism to prolong the life span from Drosophila to humans.

show abstract

Section: Discussionmentioning

confidence: 87%

Transcriptome evidence reveals enhanced autophagy-lysosomal function in centenarians

Xiao

Chen

et al. 2018

Genome Res.

View full text Add to dashboard Cite

show abstract

“…REDD1 inhibits the interaction of TSC2 with 14-3-3, resulting in greater TSC2 dependent inhibition of mTORC1 [177]. Although the role of REDD1 in the heart has not been fully examined, REDD1 knockdown impairs autophagy in hypertrophied cardiomyocytes [178]. In addition to mTORC1 regulation, a recent study discovered that REDD1 forms a complex with TXNIP, a pro-oxidant protein, and induces ROS, suppresses ATG4B activity and activates autophagy [179].…”

Section: Nutrient Sensing Regulation Of Mtorc1mentioning

confidence: 99%

Nutrient-sensing mTORC1: Integration of metabolic and autophagic signals

Tan

Miyamoto

2016

Journal of Molecular and Cellular Cardiology

View full text Add to dashboard Cite

The ability of adult cardiomyocytes to regenerate is limited, and irreversible loss by cell death plays a crucial role in heart diseases. Autophagy is an evolutionary conserved cellular catabolic process through which long-lived proteins and damaged organelles are targeted for lysosomal degradation. Autophagy is important in cardiac homeostasis and can serve as a protective mechanism by providing an energy source, especially in the face of sustained starvation. Cellular metabolism is closely associated with cell survival, and recent evidence suggests that metabolic and autophagic signaling pathways exhibit a high degree of crosstalk and are functionally interdependent. In this review, we discuss recent progress in our understanding of regulation of autophagy and its crosstalk with metabolic signaling, with a focus on the nutrient-sensing mTOR complex1 (mTORC1) pathway.

show abstract

“…Accumulated data have shown that dysfunction of autophagy is associated with development of cardiac hypertrophy [2,5]. Importantly, activation of autophagy by pharmacotherapy or gene modification can retard development of hypertrophy and protect cardiac function [6,7]. Thus, therapy to preserve autophagic regulation may represent a new and useful strategy for management of cardiac hypertrophy.…”

Section: Introductionmentioning

confidence: 97%

Puerarin prevents cardiac hypertrophy induced by pressure overload through activation of autophagy

Liu

et al. 2015

Biochemical and Biophysical Research Communications

View full text Add to dashboard Cite

REDD1 attenuates cardiac hypertrophy via enhancing autophagy

Cited by 34 publications

References 32 publications

Transcriptome evidence reveals enhanced autophagy-lysosomal function in centenarians

Transcriptome evidence reveals enhanced autophagy-lysosomal function in centenarians

Nutrient-sensing mTORC1: Integration of metabolic and autophagic signals

Puerarin prevents cardiac hypertrophy induced by pressure overload through activation of autophagy

Contact Info

Product

Resources

About