Tissue engineering holds immense promise to revolutionize regenerative medicine by enabling the fabrication of functional, patient-specific tissues and organs for clinical translation, yet it continues to face persistent challenges in designing scaffolds that simultaneously recapitulate native tissue architecture, support cell viability, and enable efficient mass transport. Traditional fabrication has moved the field forward, yet routinely falls short of producing hierarchical, anisotropic, biomimetic structures under gentle conditions. Ice-templating (or freeze-casting), which is based on freeze-induced microphase separation, reframes the problem as crystal-growth engineering. This review summarizes current fabrication strategies and their underlying mechanism of ice-templating technology from physical and chemical perspectives. We then highlight recent advances in ice-templating for tissue engineering application fields such as 3D cell culture, wound healing, bone regeneration, nerve repair, and liver support, emphasizing the relationship between microstructure and biomedical functional performance. Finally, we discuss the key challenges in translating ice-templated biomaterials from laboratory research to clinical practice and outline future directions to fully harness this versatile biomedical strategy.

The reprogramming of tumor-associated macrophages (TAMs) from a pro-tumoral M2 to an anti-tumoral M1 phenotype is an attractive therapeutic strategy whose clinical translation is undermined by the systemic toxicity of currently available pharmacological approaches. Here, we demonstrate that non-invasive and localizable pulsed electromagnetic fields (PEMFs) induce macrophage reprogramming downstream of transient receptor potential canonical 1 (TRPC1) channel activation. Brief (10 min) PEMF exposure polarized macrophages toward an M1 phenotype by activating Stimulator of Interferon Genes (STING)-dependent NF-κB inflammatory pathways that were abolished by TRPC1 knockdown or inhibition. PEMF exposure directly enhanced the immunogenicity of breast cancer cells and modified macrophage-cancer crosstalk to promote M1 macrophage polarization and the attraction of STING-activated macrophages to the cancer cells. In co-cultures, PEMF exposure stimulated macrophage-mediated phagocytosis of cancer cells in a STING- and TRPC1-dependent manner. In spheroids, PEMFs induced the reprogramming of TAMs to an M1 status and selectively enhanced infiltration of M1 macrophages, resulting in STING-mediated phagocytosis of cancer cells. In mice, 2 weeks of twice-weekly PEMF exposure resorbed engrafted tumors and selectively eliminated cancer cells within tumors while promoting immune cell recruitment. PEMFs offer a non-invasive manner to locally reprogram TAMs within the tumor microenvironment to preferentially eliminate cancer cells.

Liquid metal (LM)-derived electronic skin (e-skin) exhibits significant potential in the domains of human-machine interfaces, health monitoring and energy management. Herein, we introduce a cost-effective paradigm of LMs-derived e-skin featuring anti-freezing capability, efficient thermal management, and motion detection. The inexpensive and eco-friendly porous pomelo pith (PP) is employed as the substrate for the patterning of LM and as the physical scaffold for adhesive hydrogels. The unique porous architecture of the PP provides a natural template for the integration of LM and hydrogels, which facilitates the creation of electronic devices with improved flexibility and adhesion. The diverse patterning of nickel (Ni)-doped LM on the rough and porous pomelo pith surface is facilitated by the attractive force of a magnetic field applied below. The adhesive pre-gel is readily drawn into the pores of the pomelo pith due to capillary action. The resulting LM/PP hydrogel electronics are capable of rapid and stable Joule heating behavior and reliable motion detection. Additionally, the incorporation of glycerol endows this e-skin with superior freezing and desiccation resistance. Thus, this facile fabrication strategy successfully integrates excellent conductivity, adhesion, and environmental resilience, offering a promising paradigm for advanced wearable electronics.

The molecular mechanisms linking premature and physiological aging remain incompletely understood. Here, we present a cross-species, multi-organ metabolic atlas of progeroid laminopathy (PL) generated through integrated lipidomic and metabolomic profiling of heart, lung, skin, and serum from Hutchinson–Gilford progeria syndrome (HGPS) mouse models and human PL cohorts. We identify organ-specific metabolic alterations, with the most pronounced changes observed in the skin at the omics level. Notably, we uncover disruption of a taurine–TCA–TUDCA cytoprotective axis, suggesting a coordinated metabolic vulnerability in PL. Serum profiling further reveals candidate circulating biomarkers, including increased LPC(18:1e) and LysoPA along with decreased D-glucose 1-phosphate and NAD. These alterations are conserved across species and, importantly, display concordant trends in independent cohorts of physiologically aged healthy individuals. This overlap indicates a partial convergence between PL-associated and normal aging-related metabolic changes. Together, our findings provide a metabolic framework for understanding PL pathophysiology and highlight clinically accessible biomarkers that warrant future longitudinal validation.

Adipose-derived stem cells (ADSCs) are central regulators of adipose tissue homeostasis and regenerative capacity. Accumulating evidence indicates that aging and obesity profoundly impair ADSC function, through progressive mitochondrial dysfunction and disrupted mitochondrial–nuclear communication. Emerging studies reveal that defects in nuclear–mitochondrial crosstalk constitute a key driver of ADSC senescence and adipose tissue aging. In this review, we synthesize recent advances in understanding the mitochondrial mechanisms underlying ADSC aging, with particular emphasis on how mitochondrial dysfunction reshapes stem cell fate decisions, metabolic plasticity, and inflammatory signaling within aged adipose niches. We further highlight mitochondria targeting therapeutic strategies that hold promise for reversing ADSC senescence. Collectively, this framework positions mitochondrial regulation as a unifying axis for ADSC rejuvenation, offering new opportunities to restore adipose tissue homeostasis and mitigate age-related metabolic dysfunction.

Synergy therapy of Chinese herbs is an effective strategy for wound repair and its further development focuses on the chronological release of specific herbs with healing proceeding. Herein, we report a novel asiatic acid/baicalein nanocarrier integrated microcapsule with spatiotemporal release feature from microfluidic electrospray for wound healing. Benefiting from advantages of both nanocarrier formulation and integration capacity of microfluidic electrospray, synthesized baicalein-tannic acid nanoparticles are integrated into the shell of microcapsule while fabricated asiatic acid liposomes are located at the core region. This design enables chronological release: baicalein is first released to kill bacteria, followed by releasing asiatic acid liposomes to enhance cell migration and granulation tissue formation. In vitro tests confirm the excellent biocompatibility, antibacterial and pro-migration property of microcapsules. The results from in vivo wound healing studies showed the outcomes of reduced inflammation and accelerated wound closure in microcapsules-treated wounds. Therefore, it is believed that this herbal microcapsule with spatiotemporal and hierarchical release of baicalein and asiatic acid is an effective therapeutic platform for clinical wound treatment.