Vitamin D in autophagy signaling for health and diseases: Insights on potential mechanisms and future perspectives

Bhutia, Sujit K.

doi:10.1016/j.jnutbio.2021.108841

Cited by 52 publications

(34 citation statements)

References 140 publications

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“…Vitamin D activates autophagy in many organs in healthy conditions to preserve homeostasis. It can also induce autophagy as protection against cell damage caused by intracellular microbial infection, oxidative stress, inflammation, aging, and cancer [ 171 ].…”

Section: Mechanisms Introductionmentioning

confidence: 99%

Vitamin D and Cancer: An Historical Overview of the Epidemiology and Mechanisms

2022

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This is a narrative review of the evidence supporting vitamin D’s anticancer actions. The first section reviews the findings from ecological studies of cancer with respect to indices of solar radiation, which found a reduced risk of incidence and mortality for approximately 23 types of cancer. Meta-analyses of observational studies reported the inverse correlations of serum 25-hydroxyvitamin D [25(OH)D] with the incidence of 12 types of cancer. Case-control studies with a 25(OH)D concentration measured near the time of cancer diagnosis are stronger than nested case-control and cohort studies as long follow-up times reduce the correlations due to changes in 25(OH)D with time. There is no evidence that undiagnosed cancer reduces 25(OH)D concentrations unless the cancer is at a very advanced stage. Meta-analyses of cancer incidence with respect to dietary intake have had limited success due to the low amount of vitamin D in most diets. An analysis of 25(OH)D-cancer incidence rates suggests that achieving 80 ng/mL vs. 10 ng/mL would reduce cancer incidence rates by 70 ± 10%. Clinical trials have provided limited support for the UVB-vitamin D-cancer hypothesis due to poor design and execution. In recent decades, many experimental studies in cultured cells and animal models have described a wide range of anticancer effects of vitamin D compounds. This paper will review studies showing the inhibition of tumor cell proliferation, dedifferentiation, and invasion together with the sensitization to proapoptotic agents. Moreover, 1,25-(OH)2D3 and other vitamin D receptor agonists modulate the biology of several types of stromal cells such as fibroblasts, endothelial and immune cells in a way that interferes the apparition of metastases. In sum, the available mechanistic data support the global protective action of vitamin D against several important types of cancer.

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Section: Mechanisms Introductionmentioning

confidence: 99%

Vitamin D and Cancer: An Historical Overview of the Epidemiology and Mechanisms

2022

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“…Previous research indicated that cell autophagy may be related to bone homeostasis ( Bhutia, 2021 ). Uro-A has been proven to modulate autophagy in both cultured cells and mouse brains.…”

Section: Resultsmentioning

confidence: 99%

Gut Metabolite Urolithin A Inhibits Osteoclastogenesis and Senile Osteoporosis by Enhancing the Autophagy Capacity of Bone Marrow Macrophages

Tao

Yang

et al. 2022

Front. Pharmacol.

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Senile osteoporosis (SOP) is a systemic bone disease that is significantly associated with age and eventually leads to deteriorated bone strength and increased fracture risk. Urolithin A (Uro-A) is a gut microbiome-derived compound that is mainly produced from pomegranates and some nuts. Uro-A has attracted great attention in recent years in view of its protective effects on aging-related diseases, including muscle dysfunction, kidney disease and knee injury. However, its protective influence and possible mechanisms in senile osteoporosis remain unclear. Our study describes the beneficial effect of Uro-A on bone marrow macrophages (BMMs). The in vitro results demonstrated that Uro-A inhibited receptor activator for nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis in BMMs in a concentration-dependent manner. Uro-A significantly reduced the expression of osteoclast-related genes and bone resorption. Mechanistically, we found that the autophagy ability of BMMs was significantly enhanced in the early stage of Uro-A treatment, accompanied by the activation of LC3 and Beclin 1. At the same time, this enhanced autophagy activity was maintained until the later stage after stimulation with RANKL. Furthermore, we found that the MARK signaling pathway was blocked by Uro-A treatment. In a mouse model of aging, Uro-A effectively inhibited bone loss in the proximal femur, spine and tibia of aging mice. These results indicated that Uro-A is a robust and effective treatment for preventing senile osteoporosis bone loss.

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“…The physiological function of VD is to control calcium homeostasis for maintaining bone mineralization. Moreover, VD can modulate innate and adaptive immunity, induce cell differentiation, apoptosis, and autophagy; inhibit cell proliferation, angiogenesis and metastasis; and regulate other cellular signaling processes ( El-Sharkawy and Malki, 2020 ; Adelani et al, 2021 ; Murdaca et al, 2021 ; Pi et al, 2021 ; Poursoltani et al, 2021 ; Zhao et al, 2021 ; Bhutia, 2022 ; Zhou et al, 2022 ). Since VD levels obtained from diet are often insufficient and VD deficiency is associated with a variety of diseases, a daily supplement of at least 25 μg (1,000 IU) of VD is recommended to prevent VD deficiency ( Holick et al, 2011 ).…”

Section: Vitamin D—metabolism Analogues and Functionsmentioning

confidence: 99%

Vitamin D: A Potential Star for Treating Chronic Pancreatitis

Zheng

Gao

2022

Front. Pharmacol.

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Chronic pancreatitis (CP) is a chronic inflammatory and fibrotic disease of the pancreas. The incidence of CP is increasing worldwide but the effective therapies are lacking. Hence, it is necessary to identify economical and effective agents for the treatment of CP patients. Vitamin D (VD) and its analogues have been confirmed as pleiotropic regulators of cell proliferation, apoptosis, differentiation and autophagy. Clinical studies show that VD deficiency is prevalent in CP patients. However, the correlation between VD level and the risk of CP remains controversial. VD and its analogues have been demonstrated to inhibit pancreatic fibrosis by suppressing the activation of pancreatic stellate cells and the production of extracellular matrix. Limited clinical trials have shown that the supplement of VD can improve VD deficiency in patients with CP, suggesting a potential therapeutic value of VD in CP. However, the mechanisms by which VD and its analogues inhibit pancreatic fibrosis have not been fully elucidated. We are reviewing the current literature concerning the risk factors for developing CP, prevalence of VD deficiency in CP, mechanisms of VD action in PSC-mediated fibrogenesis during the development of CP and potential therapeutic applications of VD and its analogues in the treatment of CP.

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Vitamin D in autophagy signaling for health and diseases: Insights on potential mechanisms and future perspectives

Cited by 52 publications

References 140 publications

Vitamin D and Cancer: An Historical Overview of the Epidemiology and Mechanisms

Vitamin D and Cancer: An Historical Overview of the Epidemiology and Mechanisms

Gut Metabolite Urolithin A Inhibits Osteoclastogenesis and Senile Osteoporosis by Enhancing the Autophagy Capacity of Bone Marrow Macrophages

Vitamin D: A Potential Star for Treating Chronic Pancreatitis

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