FibROAD: a manually curated resource for multi-omics level evidence integration of fibrosis research.

Organ fibrosis represents a vital health threat that substantially contributes to yearly mortality rates. While a considerable amount of research has been conducted on fibrosis, these reports have only focused on specific organs as affected within distinct disorders. Accordingly, results from such studies have been unable to provide a comprehensive understanding of the pathological processes involved.

Single-cell RNA-seq reveals fibroblast heterogeneity and increased mesenchymal fibroblasts in human fibrotic skin diseases.

Fibrotic skin disease represents a major global healthcare burden, characterized by fibroblast hyperproliferation and excessive accumulation of extracellular matrix. Fibroblasts are found to be heterogeneous in multiple fibrotic diseases, but fibroblast heterogeneity in fibrotic skin diseases is not well characterized. In this study, we explore fibroblast heterogeneity in keloid, a paradigm of fibrotic skin diseases, by using single-cell RNA-seq.

TRAF4 Promotes Fibroblast Proliferation in Keloids by Destabilizing p53 via Interacting with the Deubiquitinase USP10.

Keloids represent one extreme of aberrant dermal wound healing. One of the important characteristics of keloids is uncontrolled fibroblasts proliferation. However, the mechanism of excessive proliferation of fibroblasts in keloids remains elusive.

RNA-seq analysis provides insight into reprogramming of culm development in Zizania latifolia induced by Ustilago esculenta.

We report a transcriptome assembly and expression profiles from RNA-Seq data and identify genes responsible for culm gall formation in Zizania latifolia induced by Ustilago esculenta. The smut fungus Ustilago esculenta can induce culm gall in Zizania latifolia, which is used as a vegetable in Asian countries. However, the underlying molecular mechanism of culm gall formation is still unclear.

Bu-Shen-Ning-Xin Decoction ameliorated the osteoporotic phenotype of ovariectomized mice without affecting the serum estrogen concentration or uterus.

Introduction: Bu-Shen-Ning-Xin Decoction (BSNXD), a traditional Chinese medicinal composition, has been used as a remedy for postmenopausal osteoporosis, but its effects on bone metabolism and the uterus have not been reported.

Purpose: We aimed to determine the respective effects of BSNXD on the bones and the uterus of ovariectomized (OVX) mice to evaluate the efficacy and safety of this herbal formula.

Materials And Methods: Postmenopausal osteoporosis animal models that were generated by ovariectomy were treated with BSNXD.

Bu-Shen-Ning-Xin decoction: inhibition of osteoclastogenesis by abrogation of the RANKL-induced NFATc1 and NF-κB signaling pathways via selective estrogen receptor α.

Introduction: Bu-Shen-Ning-Xin decoction (BSNXD) is a traditional Chinese medicinal composition that has been used as a remedy for postmenopausal osteoporosis, but the mechanisms affecting bone metabolism are not fully understood.

Purpose: We investigated the molecular mechanism and signaling pathway underlying the effect of BSNXD on osteoclastogenesis.

Materials And Methods: A postmenopausal osteoporosis animal model generated by ovariectomy was administered BSNXD and drug-derived serum was prepared.

BSNXD modulates mesenchymal stem cell differentiation into osteoblasts in a postmenopausal osteoporotic mouse model.

Mesenchymal stem cells (MSCs) are a type of stem cell that has multidirectional differentiation abilities. Under certain inducing factors, MSCs can differentiate into osteoblasts and adipocytes. Adipocytes and osteoblasts are derived from MSCs, and decreased osteoblastogenesis and increased adipocytes may be a primary cause of postmenopausal osteoporosis (PMO).

Aging affects epidermal Langerhans cell development and function and alters their miRNA gene expression profile.

Immunosenescence is a result of progressive decline in immune system function with advancing age. Epidermal Langerhans cells (LCs), belonging to the dendritic cell (DC) family, act as sentinels to play key roles in the skin immune responses. However, it has not been fully elucidated how aging affects development and function of LCs.

Lack of microRNA miR-150 reduces the capacity of epidermal Langerhans cell cross-presentation.

MicroRNAs (miRNAs) are evolutionarily conserved small non-coding RNAs that repress target genes at post-transcriptional level. Langerhans cells (LCs) are skin-residential dendritic cells (DCs) with a life cycle distinct from other types of DCs. miRNA deficiency interrupts the homoeostasis and function of epidermal LCs, suggesting the critical roles of miRNAs in LC development and function.

Deletion of microRNA miR-223 increases Langerhans cell cross-presentation.

Langerhans cells (LCs) are skin-residential dendritic cells that regulate skin immunity. MicroRNAs (miRNAs) are key regulators in the control of biological functions in a variety of cell types. Deletion of all miRNAs interrupts the homeostasis and function of epidermal LCs.

[Anti-tumor effects of 10-hydroxycamptothecinc-treated DC-Hepa1-6 fusion vaccines].

Objective: To investigate the induction of antitumor immune responses and therapeutic effects of 10-hydroxycamptothecinc-treated (HCPT) DC-Hepa fusion vaccines by DC fused with hepal-6 cell from hepatoma.

Methods: The fused cells were isolated by magnetic cell sorting and adherent culture. Cell apoptosis was detected by Rhodamine123/PI double-labeled assay, CTL activity by 4 h (51)Cr releasing assay.