scholarly journals Boosting the Photoaged Skin: The Potential Role of Dietary Components

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1691
Author(s):  
Ruixuan Geng ◽  
Seong-Gook Kang ◽  
Kunlun Huang ◽  
Tao Tong

Skin photoaging is mainly induced by ultraviolet (UV) irradiation and its manifestations include dry skin, coarse wrinkle, irregular pigmentation, and loss of skin elasticity. Dietary supplementation of nutraceuticals with therapeutic and preventive effects against skin photoaging has recently received increasing attention. This article aims to review the research progress in the cellular and molecular mechanisms of UV-induced skin photoaging. Subsequently, the beneficial effects of dietary components on skin photoaging are discussed. The photoaging process and the underlying mechanisms are complex. Matrix metalloproteinases, transforming growth factors, skin adipose tissue, inflammation, oxidative stress, nuclear and mitochondrial DNA, telomeres, microRNA, advanced glycation end products, the hypothalamic–pituitary–adrenal axis, and transient receptor potential cation channel V are key regulators that drive the photoaging-associated changes in skin. Meanwhile, mounting evidence from animal models and clinical trials suggests that various food-derived components attenuate the development and symptoms of skin photoaging. The major mechanisms of these dietary components to alleviate skin photoaging include the maintenance of skin moisture and extracellular matrix content, regulation of specific signaling pathways involved in the synthesis and degradation of the extracellular matrix, and antioxidant capacity. Taken together, the ingestion of food-derived functional components could be an attractive strategy to prevent skin photoaging damage.

2015 ◽  
Vol 29 (11) ◽  
pp. 4726-4737 ◽  
Author(s):  
Felix Kurth ◽  
Alfredo Franco‐Obregón ◽  
Marco Casarosa ◽  
Simon K. Küster ◽  
Karin Wuertz‐Kozak ◽  
...  

2021 ◽  
Author(s):  
Javier Casas ◽  
Clara Meana ◽  
José Ramón López-López ◽  
Jesús Balsinde ◽  
María A. Balboa

ABSTRACTToll-like receptor 4, the receptor for bacterial lipopolysaccharide (LPS), drives inflammatory responses that protect against pathogens and boost the adaptive immunity. LPS responses are known to depend on calcium fluxes, but the molecular mechanisms involved are poorly understood. Here we present evidence that the transient receptor potential canonical channel 3 (TRPC3) is activated intracellularly during macrophage exposure to LPS and is essential for Ca2+ release from internal stores. In this way TRPC3 participates in cytosolic Ca2+ elevations, TLR4 endocytosis, activation of inflammatory transcription factors and cytokine upregulation. We also report that TRPC3 is activated by diacylglycerol (DAG) generated by the phosphatidic acid phosphatase lipin-1. In accord with this, lipin-1-deficient cells show reduced Ca2+ responses to LPS challenge. A cameleon indicator directed to the endoplasmic reticulum shows that this is the organelle from which TRPC3 mediates the Ca2+ release. Finally, pharmacological inhibition of TRPC3 reduces systemic inflammation induced by LPS in mice. Collectively, our study unveils a central component of LPS-triggered Ca2+ signaling that involves intracellular sensing of lipin-1-derived DAG by TRPC3.


2020 ◽  
Vol 2020 ◽  
pp. 1-13 ◽  
Author(s):  
Zhi-Chuan Sun ◽  
Sui-Bin Ma ◽  
Wen-Guang Chu ◽  
Dong Jia ◽  
Ceng Luo

Chronic pathological pain is one of the most intractable clinical problems faced by clinicians and can be devastating for patients. Despite much progress we have made in understanding chronic pain in the last decades, its underlying mechanisms remain elusive. It is assumed that abnormal increase of calcium levels in the cells is a key determinant in the transition from acute to chronic pain. Exploring molecular players mediating Ca2+ entry into cells and molecular mechanisms underlying activity-dependent changes in Ca2+ signaling in the somatosensory pain pathway is therefore helpful towards understanding the development of chronic, pathological pain. Canonical transient receptor potential (TRPC) channels form a subfamily of nonselective cation channels, which permit the permeability of Ca2+ and Na+ into the cells. Initiation of Ca2+ entry pathways by these channels triggers the development of many physiological and pathological functions. In this review, we will focus on the functional implication of TRPC channels in nociception with the elucidation of their role in the detection of external stimuli and nociceptive hypersensitivity.


Author(s):  
Bhupesh Vaidya ◽  
Shyam Sunder Sharma

Parkinson’s disease (PD) is a neurodegenerative disorder characterized by the symptoms of motor deficits and cognitive decline. There are a number of therapeutics available for the treatment of PD, but most of them suffer from serious side effects such as bradykinesia, dyskinesia and on-off effect. Therefore, despite the availability of these pharmacological agents, PD patients continue to have an inferior quality of life. This has warranted a need to look for alternate strategies and molecular targets. Recent evidence suggests the Transient Receptor Potential (TRP) channels could be a potential target for the management of motor and non-motor symptoms of PD. Though still in the preclinical stages, agents targeting these channels have shown immense potential in the attenuation of behavioral deficits and signaling pathways. In addition, these channels are known to be involved in the regulation of ionic homeostasis, which is disrupted in PD. Moreover, activation or inhibition of many of the TRP channels by calcium and oxidative stress has also raised the possibility of their paramount involvement in affecting the other molecular mechanisms associated with PD pathology. However, due to the paucity of information available and lack of specificity, none of these agents have gone into clinical trials for PD treatment. Considering their interaction with oxidative stress, apoptosis and excitotoxicity, TRP channels could be considered as a potential future target for the treatment of PD.


2006 ◽  
Vol 85 (10) ◽  
pp. 900-904 ◽  
Author(s):  
C.-K. Park ◽  
H.Y. Li ◽  
K.-Y. Yeon ◽  
S.J. Jung ◽  
S.-Y. Choi ◽  
...  

Although eugenol is widely used in dentistry, little is known about the molecular mechanisms responsible for its anesthetic properties. In addition to calcium channels, recently demonstrated by our group, there could be another molecular target for eugenol. Using a whole-cell patch-clamp technique, we investigated the effect of eugenol on voltage-gated sodium channel currents ( I Na) in rat dental primary afferent neurons identified by retrograde labeling with a fluorescent dye in maxillary molars. Eugenol inhibited action potentials and I Na in both capsaicin-sensitive and capsaicin-insensitive neurons. The pre-treatment with capsazepine, a competitive antagonist of transient receptor potential vanilloid 1 (TRPV1), failed to block the inhibitory effect of eugenol on I Na, suggesting no involvement of TRPV1. Two types of I Na, tetrodotoxin (TTX)-resistant and TTX-sensitive I Na, were inhibited by eugenol. Our results demonstrated that eugenol inhibits I Na in a TRPV1-independent manner. We suggest that I Na inhibition by eugenol contributes to its analgesic effect.


2019 ◽  
Vol 20 (3) ◽  
pp. 526 ◽  
Author(s):  
Mohammad Hossain ◽  
Marina Bakri ◽  
Farhana Yahya ◽  
Hiroshi Ando ◽  
Shumpei Unno ◽  
...  

Dental pain is a common health problem that negatively impacts the activities of daily living. Dentine hypersensitivity and pulpitis-associated pain are among the most common types of dental pain. Patients with these conditions feel pain upon exposure of the affected tooth to various external stimuli. However, the molecular mechanisms underlying dental pain, especially the transduction of external stimuli to electrical signals in the nerve, remain unclear. Numerous ion channels and receptors localized in the dental primary afferent neurons (DPAs) and odontoblasts have been implicated in the transduction of dental pain, and functional expression of various polymodal transient receptor potential (TRP) channels has been detected in DPAs and odontoblasts. External stimuli-induced dentinal tubular fluid movement can activate TRP channels on DPAs and odontoblasts. The odontoblasts can in turn activate the DPAs by paracrine signaling through ATP and glutamate release. In pulpitis, inflammatory mediators may sensitize the DPAs. They could also induce post-translational modifications of TRP channels, increase trafficking of these channels to nerve terminals, and increase the sensitivity of these channels to stimuli. Additionally, in caries-induced pulpitis, bacterial products can directly activate TRP channels on DPAs. In this review, we provide an overview of the TRP channels expressed in the various tooth structures, and we discuss their involvement in the development of dental pain.


Nutrients ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 333 ◽  
Author(s):  
Adriana Nowak ◽  
Małgorzata Zakłos-Szyda ◽  
Janusz Błasiak ◽  
Agnieszka Nowak ◽  
Zhuo Zhang ◽  
...  

Schisandra chinensis (Turcz.) Baill. (SCE) is a plant with high potential for beneficial health effects, confirmed by molecular studies. Its constituents exert anti-cancer effects through the induction of cell cycle arrest and apoptosis, as well as inhibition of invasion and metastasis in cancer cell lines and experimental animals. SCE displays antimicrobial effects against several pathogenic strains. It has anti-diabetic potential, supported by hypoglycemic activity. A diet rich in SCE improves pancreatic functions, stimulates insulin secretion, and reduces complications in diabetic animals. SCE prevents lipid accumulation and differentiation of preadipocytes, indicating its anti-obesity potential. SCE exerts a protective effect against skin photoaging, osteoarthritis, sarcopenia, senescence, and mitochondrial dysfunction, and improves physical endurance and cognitive/behavioural functions, which can be linked with its general anti-aging potency. In food technology, SCE is applied as a preservative, and as an additive to increase the flavour, taste, and nutritional value of food. In summary, SCE displays a variety of beneficial health effects, with no side effects. Further research is needed to determine the molecular mechanisms of SCE action. First, the constituents responsible for its beneficial effects should be isolated and identified, and recommended as preventative nutritional additives, or considered as therapeutics.


Cells ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 1376 ◽  
Author(s):  
Kim ◽  
Park ◽  
Choi ◽  
Kong ◽  
Kang

Transient receptor potential canonical channel-6 (TRPC6) is one of the Ca2+-permeable non-selective cation channels. TRPC6 is mainly expressed in dentate granule cell (DGC), which is one of the most resistant neuronal populations to various harmful stresses. Although TRPC6 knockdown evokes the massive DGC degeneration induced by status epilepticus (a prolonged seizure activity, SE), the molecular mechanisms underlying the role of TRPC6 in DGC viability in response to SE are still unclear. In the present study, hyperforin (a TRPC6 activator) facilitated mitochondrial fission in DGC concomitant with increases in Lon protease-1 (LONP1, a mitochondrial protease) expression and extracellular-signal-regulated kinase 1/2 (ERK1/2) phosphorylation under physiological conditions, which were abrogated by U0126 (an ERK1/2 inhibitor) co-treatment. TRPC6 knockdown showed the opposite effects on LONP1 expression, ERK1/2 activity, and mitochondrial dynamics. In addition, TRPC6 siRNA and U0126 evoked the massive DGC degeneration accompanied by mitochondrial elongation following SE, independent of seizure severity. However, LONP1 siRNA exacerbated SE-induced DGC death without affecting mitochondrial length. These findings indicate that TRPC6-ERK1/2 activation may increase DGC invulnerability to SE by regulating LONP1 expression as well as mitochondrial dynamics. Therefore, TRPC6-ERK1/2-LONP1 signaling pathway will be an interesting and important therapeutic target for neuroprotection from various neurological diseases.


Molecules ◽  
2020 ◽  
Vol 25 (9) ◽  
pp. 2222
Author(s):  
Lara Saftić Martinović ◽  
Željka Peršurić ◽  
Krešimir Pavelić

Nutrigenomics is a discipline that studies the effects of various dietary components on gene expression and molecular mechanisms via “omics” technologies. Many studies are focused on revealing the pathways of the anticancer properties of various nutraceuticals. However, it has been shown that metastasis, a multifactorial disease that develops from primary tumors in cascades, is responsible for almost 90% of cancer deaths. Regrettably, the effects of consumption of different nutraceuticals on metastasis development have not yet been sufficiently explored. A few studies on the subject have revealed the promotional effects of some nutraceuticals on metastasis development. Additionally, it has been shown that certain compounds can have beneficial effects on reduction of the primary tumor, but afterwards promote the spread of metastases. Therefore, in this review we discuss results published in the past five years focused on the effects of different nutraceuticals on metastasis development.


Physiology ◽  
2008 ◽  
Vol 23 (1) ◽  
pp. 32-40 ◽  
Author(s):  
Joost G. J. Hoenderop ◽  
René J. M. Bindels

Significant progress has been made into our understanding of the molecular mechanisms responsible for Ca2+ and Mg2+ homeostasis. Members of the transient receptor potential channel (TRP) superfamily proved essential to the maintenance of divalent cation levels by regulating their absorption from renal and intestinal lumina. This review highlights the molecular and functional aspects of these new calciotropic and magnesiotropic TRPs in health and disease.


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