The cover image is based on the article Splicing control by PHF5A is crucial for melanoma cell survival by Anja Katrin Bosserhoff et al., https://doi.org/10.1111/cpr.13741.

This review highlights the use of pluripotent stem cell-derived macrophages (PSCdMϕs) in modelling and treating infectious diseases and explores methods to create self-renewing macrophages (SRMϕs). We further propose that pluripotent stem cells can be utilized as a gene editing platform to develop self-renewing macrophages (PSRMϕs).

This work investigates the role of the splicing factor PHD Finger Protein 5A (PHF5A) in melanoma progression. PHF5A is upregulated in melanoma cells, leading to an increased splicing rate, which ensures the tumour typical high proliferation rate and apoptosis resistance. An inhibition of PHF5A results in splicing defects, inhibited proliferation and increased apoptosis by UPR activation.

Under soft matrix stiffness, lysosomes make more contacts with mitochondria through disorganized cytoskeleton, leading to calcium ion transfer and subsequently causing mitochondrial redox imbalance. Additionally, M-L contact results in imbalanced mitochondrial fission dynamics, ultimately leading to the aging of MSCs.

In this study, OP-ASCs were successfully isolated and cultured from the inguinal fat of the OP mouse with bilateral ovariotomy (OVX). Activation of the canonical Wnt signalling pathway markedly enhanced osteogenesis in OP-ASCs, concurrently suppressing Wnt5a and GSK-3β expression. Lentiviral-mediated silenced of Wnt5a could enhance the osteogenic ability of OP-ASCs by activating the canonical Wnt signalling pathway to promote the repair of critical-sized calvarial defects in osteoporotic mice.

Severe acute respiratory syndrome coronavirus (SARS-CoV-2) infection can cause hypoxia at the maternal–fetal interface in the first trimester, resulting in differential gene expression in different cells and metabolic abnormalities, which are weakened but persist in the second trimester.

Our study characterized the retinal phenotypes of Tmem184b KO mice and confirmed the underlying mechanisms including cell death, inflammation and response to hypoxia pathway for retinal degeneration (RD) in the absence of TMEM184B, providing a rationale for therapeutic and diagnostic applications of RD.

Notch-1 activation (NICD) inhibits collective cell migration by promoting high intracellular force and strong cell–cell adhesion. Notch-1 activation leads to GSK-3β activity by inhibiting ILK phosphorylation, β- catenin is degraded and cannot enter the nucleus, resulting in higher expression of E-cadherin and tighter intercellular connections. Additionally, Notch-1 stimulates the Rho/ROCK pathway, which enhances adhesions between cells and the extracellular matrix and ultimately impedes collective cell migration.

Single-cell RNA-seq analysis dynamic transcriptomic and regulatory networks underpinning the transition from fetal primordial germ cells to spermatogonia in mice.

KDM2B promote the neurogenesis of stem cells from apical papilla (SCAP), through up-regulating mitogen-activated protein kinase-1 (MAP2K1), PBX3, Neuregulin-1 (NRG1), neurofilament heavy (NEFH) and Cadherin-2 (CDH2) via H3K4me3 methylation. Enhancer of zeste homologue 2 (EZH2) inhibited the neurogenic differentiation in SCAP, and was negatively regulated by KDM2B during neurogenic induction. KDM2B interacted with EZH2, and the binding between KDM2B and EZH2 was decreased during neurogenic induction. KDM2B-peptides were synthesized basing on KDM2B binding sequences with EZH2. By using KDM2B-peptides, the binding of EZH2 with KDM2B was effectively decreased. And KDM2B-peptides promoted the neurogenic differentiation ability of SCAP by intervening EZH2 function. The usage of KDM2B-peptides treated SCAP improved the motor ability of SCI rats.

We show that the intestinal microRNA (miR)-27a-3p is an important regulator of intestinal epithelial cell proliferation and enterocyte differentiation. Repression of endogenous miR-27a-3p leads to increased enterocyte differentiation and decreased intestinal epithelial cell proliferation in mouse and human small intestinal organoids.

GDNF promotes intestinal wound healing by promoting cell proliferation. This is mediated by RET-dependent activation of Src kinase with consecutive LGR5 upregulation, indicating activation of the stem cell niche.

SIRT7-mediated crotonylation (Kr) of minichromosome maintenance 6 (MCM6) induced DNA replication stress and regulated by RNF8-mediated ubiquitination. Kaempferol, which acted as a regulator of SIRT7, could enhance MCM6 Kcr level, alleviating tumour weight, especially combined with paclitaxel, which presents a potential chemotherapeutic target for BRCA therapy.

JNK signalling plays a critical role in Sertoli cells development and functional maintenance. Disruption of JNK signalling leads to polarity loss and cell senescence in Sertoli cells, resulting in aberrant testis development and male infertility in mouse models.

Human primed embryonic stem cells drived EXMCs by activating the Wnt pathway showed EXMC characteristics and the sorted EXMCs were able to generate significant quantities of ECM proteins and E-MSCs in the process of chondrogenesis and osteogenesis.

This study used periodically heated brain organoids derived from hPSCs to model prenatal heat exposure. It explored effects on size, neural tube development, gene expression, proliferation and differentiation, and their implications for neurodevelopmental disorders.