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Bioactive Compounds in Inflammations and Aging Diseases: Molecular Mechanisms and Therapeutic Roles

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Bioactives and Nutraceuticals".

Deadline for manuscript submissions: 30 July 2024 | Viewed by 1825

Special Issue Editor


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Guest Editor
Department of Patho-Biochemistry, Faculty of Pharmaceutical Sciences, Sanyo-Onoda City University, 1-1-1 Daigaku-Doori, Sanyo-Onoda, Yamaguchi 756-0884, Japan
Interests: extracellular matrix; matricellular protein; cell adhesion; tenascin-C; TNIIIA2; fibronectin; FNIII14; β1-integrin; macrophage; chronic inflammation; cellular senescence; age-related diseases

Special Issue Information

Dear Colleagues,

In addition to the rapidly growing elderly population worldwide, the continuous increase in morbidity of age-related diseases has become a big issue, especially in modern society. Fortunately, we are able to designate a standard of clinical care toward these diseases; however, we still cannot not control them completely.

Age-related diseases consist of various diseases. Conditions representatives of them include cancer, metabolic disease, atherosclerosis, neurodegenerative disease, arthritis and so on. In the past few decades, it has become widely accepted that these diseases are defined as inflammatory diseases overall. Chronic inflammation, which is frequently observed in the lesions of age-related disease, commonly contributes to establishing the molecular basis for disease promotion and progression. Thus, to seek a new molecular target and/or new strategies for clinical treatment, researchers are trying to unveil key molecular mechanisms triggering the expression of abnormal cellular functions, followed by progression of inflammation and formation of disease lesion, day and night.

The aims of this Special Issue are to highlight and introduce novel observations in the molecular mechanism underlying inflammatory age-related diseases, and/or findings in the new tools for managing pathological conditions. Fruitful information would be assembled in this issue. We especially welcome submissions of original research articles, short communications, and reviews from experts in age-related diseases and relevant research field.

Dr. Takuya Iyoda
Guest Editor

Manuscript Submission Information

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Keywords

  • molecular mechanism
  • inflammation
  • age-related diseases
  • cancer
  • atherosclerosis
  • metabolic disease
  • neurodegenerative disease
  • arthritis
  • cellular senescence
  • abnormal cellular function
  • new clinical strategy

Published Papers (2 papers)

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Research

14 pages, 3241 KiB  
Article
Bioactive TNIIIA2 Sequence in Tenascin-C Is Responsible for Macrophage Foam Cell Transformation; Potential of FNIII14 Peptide Derived from Fibronectin in Suppression of Atherosclerotic Plaque Formation
by Takuya Iyoda, Asayo Ohishi, Yunong Wang, Miyabi-Shara Yokoyama, Mika Kazama, Naoyuki Okita, Sachiye Inouye, Yoshimi Nakagawa, Hitoshi Shimano and Fumio Fukai
Int. J. Mol. Sci. 2024, 25(3), 1825; https://doi.org/10.3390/ijms25031825 - 02 Feb 2024
Viewed by 743
Abstract
One of the extracellular matrix proteins, tenascin-C (TN-C), is known to be upregulated in age-related inflammatory diseases such as cancer and cardiovascular diseases. Expression of this molecule is frequently detected, especially in the macrophage-rich areas of atherosclerotic lesions; however, the role of TN-C [...] Read more.
One of the extracellular matrix proteins, tenascin-C (TN-C), is known to be upregulated in age-related inflammatory diseases such as cancer and cardiovascular diseases. Expression of this molecule is frequently detected, especially in the macrophage-rich areas of atherosclerotic lesions; however, the role of TN-C in mechanisms underlying the progression of atherosclerosis remains obscure. Previously, we found a hidden bioactive sequence termed TNIIIA2 in the TN-C molecule and reported that the exposure of this sequence would be carried out through limited digestion of TN-C by inflammatory proteases. Thus, we hypothesized that some pro-atherosclerotic phenotypes might be elicited from macrophages when they were stimulated by TNIIIA2. In this study, TNIIIA2 showed the ability to accelerate intracellular lipid accumulation in macrophages. In this experimental condition, an elevation of phagocytic activity was observed, accompanied by a decrease in the expression of transporters responsible for lipid efflux. All these observations were mediated through the induction of excessive β1-integrin activation, which is a characteristic property of the TNIIIA2 sequence. Finally, we demonstrated that the injection of a drug that targets TNIIIA2’s bioactivity could rescue mice from atherosclerotic plaque expansion. From these observations, it was shown that TN-C works as a pro-atherosclerotic molecule through an internal TNIIIA2 sequence. The possible advantages of clinical strategies targeting TNIIIA2 are also indicated. Full article
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12 pages, 2635 KiB  
Article
Polysaccharide from Artocarpus heterophyllus Lam. (Jackfruit) Pulp Ameliorates Dextran Sodium Sulfate-Induced Enteritis in Rats
by Yunlong Li, Yuzi Chen, Chuan Li, Gang Wu, Yanfu He, Lehe Tan and Kexue Zhu
Int. J. Mol. Sci. 2024, 25(3), 1661; https://doi.org/10.3390/ijms25031661 - 29 Jan 2024
Cited by 1 | Viewed by 683
Abstract
A polysaccharide from Artocarpus heterophyllus Lam. (jackfruit) pulp (JFP-Ps) is known for its excellent bioactivities. However, its impact on small intestinal barrier function is still largely unexplored. The study aimed to examine the protection effect of JFP-Ps against dextran sodium sulfate-induced enteritis and [...] Read more.
A polysaccharide from Artocarpus heterophyllus Lam. (jackfruit) pulp (JFP-Ps) is known for its excellent bioactivities. However, its impact on small intestinal barrier function is still largely unexplored. The study aimed to examine the protection effect of JFP-Ps against dextran sodium sulfate-induced enteritis and its underlying mechanism. This research revealed that JFP-Ps mitigated small intestinal tissue damage by reducing the expression of pro-inflammatory cytokines and promoting the expression of the anti-inflammatory cytokine interleukin-10 in the small intestine. JFP-Ps diminished oxidative stress by bolstering the activity of antioxidant enzymes and reducing the concentration of malondialdehyde in the small intestine. In addition, JFP-Ps may restore the mechanical barrier and inhibit intestinal structure damage by augmenting the expression of short-chain fatty acids (SCFAs) receptors (GPR41/43) and up-regulating the expression of tight junction proteins (occludin). In conclusion, JFP-Ps may positively influence intestinal health by relieving oxidative stress in the small intestine, improving mechanical barrier function, activating the SCFA-GPR41/GPR43 axis, and inhibiting TLR4/MAPK pathway activation. The results augment our comprehension of the bioactivities of JFP-Ps, corroborating its great potential as a functional food. Full article
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