Shikimic acid protects skin cells from UV-induced senescence through activation of the NAD+-dependent deacetylase SIRT1

Martínez-Gutiérrez, Alfredo; Fernández-Duran, Irene; Marazuela-Duque, Anna; Simonet, Nicolas G.; Yousef, Ibraheem; Martínez-Rovira, I.; Martínez-Hoyos, Josefina; Vaquero, Alejandro

doi:10.18632/aging.203010

Cited by 12 publications

(8 citation statements)

References 82 publications

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“…However, the research of trans-resveratrol on cardiovascular protection is still rare. Other compounds in SGR also have an anti-oxidative effect, including that Shikimic acid could reduce the accumulation of ROS to modulate oxidative stress and apoptosis in Kidneys, and Shikimic acid could reverse H 2 O 2 -induced cellular oxidative damage via JNK/Bax pathway to reduce cellular damage ( Manna et al, 2014 ; Rabelo et al, 2015 ; Lee et al, 2020 ; Martinez-Gutierrez et al, 2021 ). Epicatechin and its metabolites could protect against oxidative stress via a direct antioxidant effect in the cardiovascular system ( Ruijters et al, 2013 ), gastrointestinal system ( Li Y. et al, 2019 ), and respiratory system ( Shariati et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

Mechanism and Protective Effect of Smilax glabra Roxb on the Treatment of Heart Failure via Network Pharmacology Analysis and Vitro Verification

Long

Huang

et al. 2022

Front. Pharmacol.

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Smilax glabra Roxb (SGR) has been widely applied alone or in combination with other Chinese herbs in heart failure (HF), but its mechanism and protective effect have not been investigated. We aimed to explore the mechanism and protective effect of SGR on the treatment of HF. Network pharmacology analysis predicted that SGR was involved in the regulation of cell proliferation, oxidation–reduction process, apoptotic process, ERK1 and ERK2 cascade, MAPK cascade, etc. Its mechanism was mainly involved in the MAPK signaling pathway, calcium signaling pathway, cardiac muscle contraction, etc. Subsequently, SGR was proved to improve cellular viability, restore cellular morphology, suppress cellular and mitochondrial ROS production, improve H2O2-induced lysosome inhibition, attenuate mitochondrial dysfunction, and protect mitochondrial respiratory and energy metabolism in H9c2 cells. SGR activated the p38MAPK pathway by decreasing the mRNA expression of AKT, PP2A, NF-KB, PP2A, RAC1, and CDC42 and increasing the mRNA expression of Jun, IKK, and Sirt1. SGR also decreased the protein expression of ERK1, ERK2, JNK, Bax, and Caspase3 and increased the protein expression of p38MAPK and Bcl-2. In addition, Istidina at the highest degree was identified in SGR via the UHPLCLTQ-Orbitrap-MSn method, and it was suggested as anti-heart failure agents by targeting SRC with molecular docking analysis. In conclusion, SGR has a protective effect on HF through cellular and mitochondrial protection via multi-compounds and multi-targets, and its mechanism is involved in activating the p38 MAPK pathway. Istidina may be possible anti-HF agents by targeting SRC.

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Section: Discussionmentioning

confidence: 99%

Mechanism and Protective Effect of Smilax glabra Roxb on the Treatment of Heart Failure via Network Pharmacology Analysis and Vitro Verification

Long

Huang

et al. 2022

Front. Pharmacol.

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“…Research efforts are now focused on understanding the context-dependent roles of autophagy and on the evaluation of the pharmacological effects of autophagy signaling in a more indepth and mechanistic way (35). Furthermore, the development of skin aging is associated with several molecular changes including the accumulation of DNA damage, genome instability, epigenetic dysregulation, mitochondrial dysfunction, inflammation, extracellular matrix degradation, loss of proteostasis, ER stress, and autophagy dysfunction (36). Many of these genome alterations are directly associated with cellular damage and senescence, which is one of the hallmarks of skin aging.…”

Section: Discussionmentioning

confidence: 99%

Pharmacological Activation of Autophagy Restores Cellular Homeostasis in Ultraviolet-(B)-Induced Skin Photodamage

et al. 2021

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Ultraviolet (UV) exposure to the skin causes photo-damage and acts as the primary etiological agent in photo-carcinogenesis. UV-B exposure induces cellular damage and is the major factor challenging skin homeostasis. Autophagy allows the fundamental adaptation of cells to metabolic and oxidative stress. Cellular dysfunction has been observed in aged tissues and in toxic insults to cells undergoing stress. Conversely, promising anti-aging strategies aimed at inhibiting the mTOR pathway have been found to significantly improve the aging-related disorders. Recently, autophagy has been found to positively regulate skin homeostasis by enhancing DNA damage recognition. Here, we investigated the geno-protective roles of autophagy in UV-B-exposed primary human dermal fibroblasts (HDFs). We found that UV-B irradiation to HDFs impairs the autophagy response in a time- and intensity-independent manner. However, improving autophagy levels in HDFs with pharmacological activators regulates the UV-B-induced cellular stress by decreasing the induction of DNA photo-adducts, promoting the DNA repair process, alleviating oxidative and ER stress responses, and regulating the expression levels of key cell cycle regulatory proteins. Autophagy also prevents HDFs from UV-B-induced nuclear damage as is evident in TUNEL assay and Acridine Orange/Ethidium Bromide co-staining. Salubrinal (an eIF2α phosphatase inhibitor) relieves ER stress response in cells and also significantly alleviates DNA damage and promotes the repair process in UV-B-exposed HDFs. P62-silenced HDFs show enhanced DNA damage response and also disturb the tumor suppressor PTEN/pAKT signaling axis in UV-B-exposed HDFs whereas Atg7-silenced HDFs reveal an unexpected consequence by decreasing the UV-B-induced DNA damage. Taken together, these results suggest that interventional autophagy offers significant protection against UV-B radiation-induced photo-damage and holds great promise in devising it as a suitable therapeutic strategy against skin pathological disorders.

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“…Several genes are thought to impact natural variations in the pace of aging. 9 Aging is not a disease, but a significant risk factor for several diseases, including sarcopenia. Future research will focus on the healthy lifespan and possible lifespan of aging-related disease interventions and determine their interaction with pathways that regulate aging.…”

Section: Systemic Factors Contributing To Sarcopeniamentioning

confidence: 99%

“…These studies suggest that genes associated with aging are species conserved. Several genes are thought to impact natural variations in the pace of aging 9 . Aging is not a disease, but a significant risk factor for several diseases, including sarcopenia.…”

Section: Current Views Of Pathogenesis For Sarcopeniamentioning

confidence: 99%

Recent advances in cell‐based and cell‐free therapeutic approaches for sarcopenia

Lin

Zhang

et al. 2022

The FASEB Journal

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Sarcopenia is a progressive loss of muscle mass and function that is connected with increased hospital expenditures, falls, fractures, and mortality. Although muscle loss has been related to aging, injury, hormonal imbalances, and diseases such as malignancies, chronic obstructive pulmonary disease, heart failure, and kidney failure, the underlying pathogenic mechanisms of sarcopenia are unclear.How to cite this article: Wu S, Lin S, Zhang X, et al. Recent advances in cell-based and cell-free therapeutic approaches for sarcopenia.

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Shikimic acid protects skin cells from UV-induced senescence through activation of the NAD+-dependent deacetylase SIRT1

Cited by 12 publications

References 82 publications

Mechanism and Protective Effect of Smilax glabra Roxb on the Treatment of Heart Failure via Network Pharmacology Analysis and Vitro Verification

Mechanism and Protective Effect of Smilax glabra Roxb on the Treatment of Heart Failure via Network Pharmacology Analysis and Vitro Verification

Pharmacological Activation of Autophagy Restores Cellular Homeostasis in Ultraviolet-(B)-Induced Skin Photodamage

Recent advances in cell‐based and cell‐free therapeutic approaches for sarcopenia

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