Aging is a major risk factor for chronic diseases, and calorie restriction (CR) is a robust non-pharmacological intervention that can extend health span in multiple species. Alternative splicing (AS) generates multiple RNA isoforms from a single pre-mRNA and becomes dysregulated with age; intriguingly, prior work suggests that CR can attenuate age-associated splicing noise. What has remained unclear is whether AS responses to CR are coordinated across tissues and whether they scale with the level of restriction.

Congenital heart defects (CHD) represent the most common congenital malformations globally and constitute a leading cause of neonatal mortality, with early maternal risk factors playing significant roles in their development. A comprehensive systematic review and meta-analysis by Zihan Suo and colleagues investigated the relationships between various maternal factors during the first trimester and the risk of CHD in offspring, providing robust evidence for public health strategies aimed at reducing CHD incidence. The study protocol was registered on PROSPERO (CRD42023476855), ensuring methodological transparency and rigor.

Chimeric antigen receptor T (CAR-T) cell therapy has emerged as a transformative approach in modern medicine, demonstrating remarkable efficacy in targeting pathogenic B-cell lineages with unprecedented specificity. Originally developed for B cell malignancies, this innovative immunotherapy has recently shown extraordinary potential in treating various autoimmune diseases by depleting autoreactive B cells and effectively resetting the immune system. The review by Qi Li and colleagues provides a comprehensive examination of the progression, clinical applications, challenges, and future directions of B cell-targeted CAR-T therapy across multiple autoimmune conditions.

Extensive bone defects pose substantial clinical challenges, frequently resulting in severe functional impairment and diminished quality of life for patients. Conventional therapeutic approaches, including autografts and allografts, remain widely utilized despite significant drawbacks such as donor site morbidity, limited availability, and potential immunogenic responses. Consequently, tissue engineering has emerged as an increasingly attractive alternative strategy. Bioceramic bone repair materials offer dual functionality by providing essential mechanical support while delivering bioactive properties that facilitate defect healing. A critical aspect of their therapeutic efficacy lies in their capacity to modulate the immune microenvironment, thereby promoting cellular behaviors and signaling pathways that favor bone regeneration. These immunoregulatory effects prove instrumental throughout the entire bone repair process and largely determine the ultimate success of regenerative outcomes. For example, hydroxyapatite demonstrates the ability to induce macrophage polarization toward the M2 phenotype, generating anti-inflammatory effects that enhance bone tissue repair. A comprehensive review published in Frontiers of Medicine systematically examines recent progress in bioceramic research for bone tissue engineering, encompassing material classification, immunomodulatory mechanisms, contemporary fabrication methodologies, and clinical translation status, with the objective of informing future investigations and improved therapeutic strategies.

Discovery reveals how drug-resistant tumours can shift into a state that responds better to chemotherapy.

Cardiovascular disease remains the leading cause of mortality worldwide, necessitating deeper insights into its molecular underpinnings beyond genetic predisposition. Epigenetic modifications, particularly methylation changes affecting DNA, proteins, and RNA, have emerged as critical regulators of gene expression implicated in cardiac pathophysiology. These heritable yet reversible chemical alterations govern chromatin architecture, transcriptional activity, and post-transcriptional processing without changing underlying nucleotide sequences. Within the spectrum of cardiovascular pathology—including ischemic heart disease, cardiac hypertrophy, heart failure, and atherosclerosis—dysregulated methylation patterns contribute substantially to disease initiation, progression, and phenotypic manifestation. Understanding the distinct and convergent roles of these three major methylation modalities offers promising avenues for developing novel diagnostic biomarkers and targeted therapeutic interventions that could transform precision medicine in cardiology.