Exercise attenuates myocardial fibrosis and increases angiogenesis-related molecules in the myocardium of aged rats

Soori, Rahman; Amini, Atoosa; Choobineh, Siroos; Eskandari, Arezoo; Behjat, Arezoo; Voltarelli, Fabrí­cio Azevedo

doi:10.1080/13813455.2019.1660370

Cited by 11 publications

(6 citation statements)

References 22 publications

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“…In aged, senescence-accelerated prone mice, voluntary wheel running was sufficient to elevate adropin concentrations to levels comparable to young, mature counterparts (170). In old rats, aerobic exercise via 15-30 minutes of treadmill running at 65-70% maximal speed, elevated adropin concentrations (25). Furthermore, old rats that underwent high-intensity interval training of 5-8 two-minute intervals at 80-100% maximal speed separated by two-minutes of active recovery at 50-60% maximal speed, increased adropin relative to the control and continuous exercise counterparts (25).…”

Section: Exercise and Adropinmentioning

confidence: 90%

“…In old rats, aerobic exercise via 15-30 minutes of treadmill running at 65-70% maximal speed, elevated adropin concentrations (25). Furthermore, old rats that underwent high-intensity interval training of 5-8 two-minute intervals at 80-100% maximal speed separated by two-minutes of active recovery at 50-60% maximal speed, increased adropin relative to the control and continuous exercise counterparts (25). Collectively, aerobic exercise increases adropin in aged models.…”

Section: Exercise and Adropinmentioning

confidence: 99%

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Role of adropin in arterial stiffening associated with obesity and type 2 diabetes

Jurrissen

Ramirez‐Perez

Cabral-Amador

et al. 2022

American Journal of Physiology-Heart and Circulatory Physiology

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Adropin is a peptide largely secreted by the liver and known to regulate energy homeostasis; however, it also exerts cardiovascular effects. Herein, we tested the hypothesis that low circulating levels of adropin in obesity and type 2 diabetes (T2D) contribute to arterial stiffening. In support of this hypothesis, we report that obesity and T2D is associated with reduced levels of adropin (in liver and plasma) and increased arterial stiffness in mice and humans. Establishing causation, we show that mesenteric arteries from adropin knockout mice are also stiffer, relative to arteries from wild-type counterparts, thus recapitulating the stiffening phenotype observed in T2D db/db mice. Given the above, we performed a set of follow-up experiments, in which we found that: 1) exposure of endothelial cells or isolated mesenteric arteries from db/db mice to adropin reduces filamentous actin (F-actin) stress fibers and stiffness; 2) adropin-induced reduction of F-actin and stiffness in endothelial cells and db/db mesenteric arteries is abrogated by inhibition of nitric oxide (NO) synthase; and 3) stimulation of smooth muscle cells or db/db mesenteric arteries with a NO mimetic reduces stiffness. Last, we demonstrated that in vivo treatment of db/db mice with adropin for four weeks reduces stiffness in mesenteric arteries. Collectively, these findings indicate that adropin can regulate arterial stiffness, likely via endothelial-derived NO, and thus support the notion that "hypoadropinemia" should be considered as a putative target for the prevention and treatment of arterial stiffening in obesity and T2D.

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Section: Exercise and Adropinmentioning

confidence: 90%

Section: Exercise and Adropinmentioning

confidence: 99%

Role of adropin in arterial stiffening associated with obesity and type 2 diabetes

Jurrissen

Ramirez‐Perez

Cabral-Amador

et al. 2022

American Journal of Physiology-Heart and Circulatory Physiology

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“…Various reports have shown that exercise training lead to NO production that can elevate the gene expression of IGF-1 and FGF-2 (56). A previous report demonstrated that FGF-2 training-induced was diminished the cardiac tissue stiffness according to the circulatory basophils reduction (15). Also, FGF-2 lead to increase eNOS activity and NO production that result in endothelial function improvement…”

Section: Discussionmentioning

confidence: 92%

The effect of combined training and resveratrol supplementation on serum levels of adropin, vascular endothelial growth factor, nitric oxide, and gene expression of fibroblast growth factor-2 and angiostatin in myocardial infarction rats

Ghasemi

Namjoo

ashabi

et al. 2023

Preprint

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Objectives: The aim of current study was evaluating the effect of exercise training and resveratrol supplementation on serum levels of adropin, vascular endothelial growth factor (VEGF), nitric oxide (NO), and gene expression of angiostatin and fibroblast growth factor-2 (FGF-2) in myocardial infarction rats Methods: 40 male Wistar rats four weeks after cardiac infarction were randomly divided into four groups: 1: control group (C-MI, n=10) 2: resveratrol group (Res-MI, n=10) 3: exercise group (Ex+MI, n=10) and 4: exercise group with resveratrol supplement (Ex+Res, n=10) were divided. The Ex+MI group and the Ex+Res group performed running on a treadmill for 10 weeks (5 sessions per week and each session lasting 50 minutes at a speed of 17 meters per minute). The serum levels of adropin, VEGF and NO were measured by ELISA method and expression of angiostatin and FGF-2 genes were measured by Real Time-PCR. The statistical analysis of the obtained data was done using the one-way analysis of variance test. Results: The findings of the present study showed that the level of NO, VEGF and adropin in EX+Res, Ex+MI and Res+Mi groups were significantly different from C-MI. Also, the difference between Ex+Res and other groups was significant. In terms of gene expression, the highest expression of FGF-2 was in the Ex+Res group and then in the Ex+MI group, and there was a significant difference between the level of Ex+Res and the Res-MI group. Also, the lowest angiotensin gene expression was in the Ex+Res and Ex+MI groups, which showed a significant difference compared to the other two groups. Conclusion: Ten weeks of aerobic exercise training and resveratrol supplementation lead to increase the levels of VEGF, adropin, NO as well as the mRNA expression of FGF-2 and decrease the levels of angiostatin in MI rat’s model.

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“…An increasing number of studies have shown that exercise training is an effective strategy to alleviate myocardial fibrosis [ 42 , 43 , 44 , 45 , 46 ]. Studies have found that aerobic exercise training reduces myocardial fibrosis by inhibiting the transforming growth factor-β1 (TGF-β1)-Smad2/3 signaling pathway and decreasing Col1 and Col3 protein expression in myocardial infarcted rats [ 43 , 47 ].…”

Section: Introductionmentioning

confidence: 99%

Aerobic Exercise Ameliorates Myocardial Fibrosis via Affecting Vitamin D Receptor and Transforming Growth Factor-β1 Signaling in Vitamin D-Deficient Mice

et al. 2023

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Myocardial fibrosis is a pathological phenomenon associated with cardiovascular disease (CVD) that plays a crucial role in the development of heart diseases. Vitamin D deficiency can promote the development of CVD and exercise plays a role in the treatment of CVD. This study aimed to explore the effects of 12-week aerobic exercise training on myocardial fibrosis in vitamin D-deficient mice. A vitamin D-deficient mouse model was induced by a vitamin D-deficient (0 IU Vitamin D3/kg) diet. Twenty-four C57BL/6J male mice were randomly divided into three groups: a control sedentary group (CONS, n = 8), a vitamin D-deficient sedentary group (VDDS, n = 8), and a vitamin D-deficient exercise group (VDDE, n = 8) which was aerobically trained for 12 weeks. The results showed that the serum 25-hydroxyvitamin D [25(OH)D] levels of the VDDS group were <50 nmol/L, which was significantly lower than that of the CONS group. Compared with the CONS group, the VDDS group showed cardiac dysfunction and significant fibrosis, together with lower vitamin D receptor (VDR) mRNA and protein expression levels, higher mRNA expression levels of profibrotic and inflammatory factors, and higher transforming growth factor-β1 (TGF-β1) and phospho-Smad2/3 (P-Smad2/3) protein expression levels. Serum 25(OH)D levels in the VDDE group were significantly higher than those in the VDDS group. Compared with the VDDS group, the VDDE group showed improved cardiac function and alleviated myocardial fibrosis. Meanwhile, the VDDE group had significantly higher VDR mRNA and protein expression levels; lower mRNA expression levels of profibrotic and inflammatory factors; and lower TGF-β1 and P-Smad2/3 protein expression levels. In conclusion, aerobic exercise training remains a promising intervention for treating myocardial fibrosis in vitamin D deficiency.

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Exercise attenuates myocardial fibrosis and increases angiogenesis-related molecules in the myocardium of aged rats

Cited by 11 publications

References 22 publications

Role of adropin in arterial stiffening associated with obesity and type 2 diabetes

Role of adropin in arterial stiffening associated with obesity and type 2 diabetes

The effect of combined training and resveratrol supplementation on serum levels of adropin, vascular endothelial growth factor, nitric oxide, and gene expression of fibroblast growth factor-2 and angiostatin in myocardial infarction rats

Aerobic Exercise Ameliorates Myocardial Fibrosis via Affecting Vitamin D Receptor and Transforming Growth Factor-β1 Signaling in Vitamin D-Deficient Mice

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