Testosterone therapy delays cardiomyocyte aging via an androgen receptor-independent pathway

Zhang, L.; Wu, Sha; Ruan, Yunjun; Li, Hong; Xing, Xiao-wen; Lai, Wenyan

doi:10.1590/s0100-879x2011007500128

Cited by 4 publications

(5 citation statements)

References 30 publications

(31 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Studies have shown that a low level of testosterone is closely related to the development of aging-associated cardiovascular disease, and testosterone replacement therapies play a beneficial role in male cardiovascular disease ( 32 , 33 ). Zhang et al ( 9 , 34 ) found that testosterone deficiency induces cardiomyocyte senescence, and physiological testosterone therapies delay cardiomyocyte senescence via an AR-independent pathway. In addition, testosterone antagonizes doxorubicin-induced cardiomyocyte senescence by modulating telomere binding factor 2 ( 9 ).…”

Section: Discussionmentioning

confidence: 99%

“…Zhang et al ( 9 , 34 ) found that testosterone deficiency induces cardiomyocyte senescence, and physiological testosterone therapies delay cardiomyocyte senescence via an AR-independent pathway. In addition, testosterone antagonizes doxorubicin-induced cardiomyocyte senescence by modulating telomere binding factor 2 ( 9 ).…”

Section: Discussionmentioning

confidence: 99%

“…Plasma testosterone level is inversely correlated with the incidence of multiple age-related diseases in elderly men (5). Some testosterone replacement therapies have suggested that testosterone is able to improve cognitive ability (6), enhance cardiac function (7), and delay cardiomyocyte senescence (8,9). Although testosterone has multiple functions, the relationship between testosterone's effect of delaying cardiomyocyte senescence and the mIGF-1/ SIRT1 pathway has not been elucidated.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Testosterone antagonizes paraquat-induced cardiomyocyte senescence via the mIGF-1/SIRT1 signaling pathway

Zheng

Cai

et al. 2020

Braz J Med Biol Res

View full text Add to dashboard Cite

Testosterone has been demonstrated to antagonize doxorubicin-induced cardiomyocyte senescence. However, whether testosterone prevents the paraquat-induced cardiomyocyte senescence is largely unknown. The detection of SA-b-gal activity was performed using senescence b-gal staining kit and the reactive oxygen species levels were determined by reactive oxygen species assay kit. The plasmids for insulin-like growth factor 1 shRNA (sh-mIGF-1), sirtuin-1 shRNA (sh-SIRT1), scramble shRNA (sh-NC), overexpressing mIGF-1 (mIGF-1), overexpressing SIRT1 (SIRT1), and negative controls (NC) were obtained for this study. The expression of target genes was detected using quantitative real-time PCR, immunolabeling, and western blot. We found that testosterone significantly delayed the paraquat-induced HL-1 cardiomyocyte senescence as evidenced by decreasing senescence-associated b-galactosidase activity and reactive oxygen species generation, which were accompanied by the up-regulated expression of mIGF-1 and SIRT1. RNA interference to reduce mIGF-1 and SIRT1 expression showed that testosterone prevented paraquat-induced HL-1 senescence via the mIGF-1/SIRT1 signaling pathway. Furthermore, myocardial contraction was evaluated by expression of genes of the contractile proteins/enzymes, such as a-myosin heavy chain 6 (MHC6), a-myosin heavy chain 7 (MHC7), a-skeletal actin (ACTA-1), and sarco/endoplasmic reticulum calcium ATPase-2 (SERCA2). Testosterone adjusted the above four gene expressions and the adjustment was blocked by mIGF-1 or SIRT1 inhibition. Our findings suggested that the mIGF-1/SIRT1 signaling pathway mediated the protective function of testosterone against the HL-1 cardiomyocyte senescence by paraquat, which provided new clues for the mechanisms underlying the antiaging role of testosterone in cardiomyocytes.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Testosterone antagonizes paraquat-induced cardiomyocyte senescence via the mIGF-1/SIRT1 signaling pathway

Zheng

Cai

et al. 2020

Braz J Med Biol Res

View full text Add to dashboard Cite

show abstract

“…Western blot was performed according to our previous method (32). Briefly, whole-cell lysates were prepared and quantified.…”

Section: Western Blotting Analysismentioning

confidence: 99%

Serum containing Buyang Huanwu decoction prevents age-associated migration and invasion of human vascular smooth muscle cells by up regulating SIRT1 expression

Zhang

Wei

Ruan

et al. 2018

BST

View full text Add to dashboard Cite

“…In addition, varying doses of testosterone impact the cardiovascular system in different ways. 18,19 …”

Section: -15mentioning

confidence: 99%

Effect of testosterone on the proliferation and collagen synthesis of cardiac fibroblasts induced by angiotensin II in neonatal rat

Yang

Wang

Yan³

et al. 2016

Bioengineered

View full text Add to dashboard Cite

The objective is to explore the effect of testosterone on the proliferation and collagen synthesis of neonatal rat cardiac fibroblasts (CF) induced by Angiotensin II (Ang II) and the underlying mechanisms. Derived from neonatal rats, the CFs were divided into 4 groups: the control group, Ang II group, testosterone group, and testosterone C Ang II group in vitro. Cell cycle distribution, collagen counts, and phosphorylated extracellular signal-regulated kinase (ERK1/2) (p -ERK1/2) expression were assessed by flow cytometry, VG staining, and immunocytochemistry, respectively. The Ang II group had a much higher proportion of cells in the S-phase, higher collagen contents, and a higher p -ERK1/2 expression level than either the control or testosterone group. However, these factors were significantly reduced in the testosterone C Ang II group as compared to the Ang II group. In terms of cells in the S-phase and the collagen contents, there was not a significant difference between the testosterone group and the control. However, the protein expression of p-ERK1/2 was significantly increased in the testosterone group as compared to the control. Testosterone inhibits the proliferation and collagen synthesis of CF induced by Ang II. The underlying mechanism may involve the ERK1/2 signaling pathway.

show abstract

Testosterone therapy delays cardiomyocyte aging via an androgen receptor-independent pathway

Cited by 4 publications

References 30 publications

Testosterone antagonizes paraquat-induced cardiomyocyte senescence via the mIGF-1/SIRT1 signaling pathway

Testosterone antagonizes paraquat-induced cardiomyocyte senescence via the mIGF-1/SIRT1 signaling pathway

Serum containing Buyang Huanwu decoction prevents age-associated migration and invasion of human vascular smooth muscle cells by up regulating SIRT1 expression

Effect of testosterone on the proliferation and collagen synthesis of cardiac fibroblasts induced by angiotensin II in neonatal rat

Contact Info

Product

Resources

About