Corrigendum to: Negligible effect of vitamin D supplementation on exacerbation in patients with chronic obstructive pulmonary disease: meta-analysis.

[This corrects the article , PMID: 37841773.].

Ferritin-mediated mitochondrial iron homeostasis is essential for the survival of hematopoietic stem cells and leukemic stem cells.

Iron metabolism plays a crucial role in cell viability, but its relationship with adult stem cells and cancer stem cells is not fully understood. The ferritin complex, responsible for intracellular iron storage, is important in this process. We report that conditional deletion of ferritin heavy chain 1 (Fth1) in the hematopoietic system reduced the number and repopulation capacity of hematopoietic stem cells (HSCs). These effects were associated with a decrease in cellular iron level, leading to impaired mitochondrial function and the initiation of apoptosis. Iron supplementation, antioxidant, and apoptosis inhibitors reversed the reduced cell viability of Fth1-deleted hematopoietic stem and progenitor cells (HSPCs). Importantly, leukemic stem cells (LSCs) derived from MLL-AF9-induced acute myeloid leukemia (AML) mice exhibited reduced Fth1 expression, rendering them more susceptible to apoptosis induced by the iron chelation compared to normal HSPCs. Modulating FTH1 expression using mono-methyl fumarate increased LSCs resistance to iron chelator-induced apoptosis. Additionally, iron supplementation, antioxidant, and apoptosis inhibitors protected LSCs from iron chelator-induced cell death. Fth1 deletion also extended the survival of AML mice. These findings unveil a novel mechanism by which ferritin-mediated iron homeostasis regulates the survival of both HSCs and LSCs, suggesting potential therapeutic strategies for blood cancer with iron dysregulation.

Negligible effect of vitamin D supplementation on exacerbation in patients with chronic obstructive pulmonary disease: meta-analysis.

Introduction: The focus of this meta-analysis was how vitamin D supplementation influences exacerbations in patients with chronic obstructive pulmonary disease (COPD) and vitamin D deficiency (VDD). Materials and methods: Cochrane Library, Web of Science, Embase, and PubMed databases have been systematically searched in an attempt to collect randomized controlled trials related to vitamin D supplementation in COPD patients with VDD published in English available by July 2022. Primary outcome indicators included the mean number of exacerbation and rate of exacerbation. Secondary outcome indicators included forced expiratory volume in the first second (FEV1), FEV1/forced vital capacity (FVC) ratio, and serum 25-hydroxyvitamin D (25(OH)D) concentration. Results: Five studies involving 522 COPD patients with VDD (defined as 25(OH)D < 50 nmol/L) were included, among them 61 were severely deficient in vitamin D (25(OH)D < 25 nmol/L). The results showed that vitamin D supplementation did not decrease the mean number of exacerbation (standardized mean difference (SMD): - 0.10, 95% CI: - 0.29 to 0.09) and the rate of exacerbation (relative risk (RR): 0.89, 95% CI: 0.76 to 1.04, P = 0.179). Also, its effect on FEV1 (SMD: - 0.06, 95% CI: - 0.30 to 0.17) and FEV1/FVC (SMD: -0.10, 95% CI: - 0.48 to 0.27) remained negligible. However, it could increase the serum 25(OH)D concentration (SMD: 2.44, 95 CI%: 2.20 to 2.68, P < 0.001). Conclusions: The effects of vitamin D supplementation on decreasing exacerbation and improving pulmonary function were not significant.

Inhibiting mitochondrial inflammation through Drp1/HK1/NLRP3 pathway: A mechanism of alpinetin attenuated aging-associated cognitive impairment.

Mitochondrial inflammation triggered by abnormal mitochondrial division and regulated by the Drp1/HK1/NLRP3 pathway is correlated with the progression of aging-associated cognitive impairment (AACI). Alpinetin is a novel flavonoid derived from Zingiberaceae that has many bioactivities such as antiinflammation and anti-oxidation. However, whether alpinetin alleviates AACI by suppressing Drp1/HK1/NLRP3 pathway-inhibited mitochondrial inflammation is still unknown. In the present study, D-galactose (D-gal)-induced aging mice and BV-2 cells were used, and the effects of alpinetin on learning and memory function, neuroprotection and activation of the Drp1/HK1/NLRP3 pathway were investigated. Our data indicated that alpinetin significantly alleviated cognitive dysfunction and neuronal damage in the CA1 and CA3 regions of D-gal-treated mice. Moreover, D-gal-induced microglial activation was markedly reduced by alpinetin by inhibiting the Drp1/HK1/NLRP3 pathway-suppressed mitochondrial inflammation, down-regulating the levels of p-Drp1 (s616), VDAC, NLRP3, ASC, Cleaved-caspase 1, IL-18, and IL-1ß, and up-regulating the expression of HK1. Furthermore, after Drp1 inhibition by Mdivi-1 in vitro, the inhibitory effect of alpinetin on Drp1/HK1/NLRP3 pathway was more evident. In summary, the current results implied that alpinetin attenuated aging-related cognitive deficits by inhibiting the Drp1/HK1/NLRP3 pathway and suppressing mitochondrial inflammation, suggesting that the inhibition of the Drp1/HK1/NLRP3 pathway is one of the mechanisms by which alpinetin attenuates AACI.