Aging is accompanied by the decline of organismal functions and a series of prominent hallmarks, including genetic and epigenetic alterations. These aging-associated epigenetic changes include DNA methylation, histone modification, chromatin remodeling, non-coding RNA (ncRNA) regulation, and RNA modification, all of which participate in the regulation of the aging process, and hence contribute to aging-related diseases. Therefore, understanding the epigenetic mechanisms in aging will provide new avenues to develop strategies to delay aging. Indeed, aging interventions based on manipulating epigenetic mechanisms have led to the alleviation of aging or the extension of the lifespan in animal models. Small molecule-based therapies and reprogramming strategies that enable epigenetic rejuvenation have been developed for ameliorating or reversing aging-related conditions. In addition, adopting health-promoting activities, such as caloric restriction, exercise, and calibrating circadian rhythm, has been demonstrated to delay aging. Furthermore, various clinical trials for aging intervention are ongoing, providing more evidence of the safety and efficacy of these therapies. Here, we review recent work on the epigenetic regulation of aging and outline the advances in intervention strategies for aging and age-associated diseases. A better understanding of the critical roles of epigenetics in the aging process will lead to more clinical advances in the prevention of human aging and therapy of aging-related diseases.

This article introduces the theories of family functions, including two kind of theory. The first is result oriented, defining family functioning by specific features of family. The second is process oriented, describing family function from the tasks families need to complete. The authors review Olson annular mode theory and Beavers system theory as representatives of result oriented family function. Then, the authors introduce McMaster family functioning mode theory and Skinner's Family process model theory as representatives of process oriented family function. At the end of this paper, the authors analyze some possible research directions in the future.

Tumortherapeutika Pyridiniumsubstituierte Tetraphenylethylen‐Salze können Autophagie induzieren und gleichzeitig den Autophagieflux hemmen. R. Zhao, D. Zhang et al. berichten in ihrem Forschungsartikel auf S. 10128, wie diese Ergebnisse neue Funktionalitäten für AIEgene aufzeigen.

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A novel metal-free, efficient cascade reaction has been developed to construct 1,2,3-triazole-fused 1,4-diazepinone skeletons. Mechanism investigation indicated that sodium azide has not only served as a 1,3-dipoles synthon in [3 + 2] cycloaddition but also prompted C−N bond formation. Furthermore, the potential utility of this protocol was demonstrated by scale-up synthesis of 1,2,3-triazole-fused diazepinone derivatives and the derivatization of them.

Tuning autophagy in a controlled manner could facilitate cancer therapy but it remains challenging. Pyridinium‐substituted tetraphenylethylene salts (PTPE 1—3), able to target mitochondria and disrupt autophagy after forming complexes with albumin, are reported. Mitochondrion affinity and autophagy‐inducing activity are improved by prolonging the length of alkyl chains in PTPE 1–3. PTPE 1–3 demonstrate proautophagic activity and a mitophagy blockage effect. Failure of autophagosome–lysosome fusion in downstream autophagy flux results in cancer cell death. Moreover, fast formation of complexes of PTPE 1–3 with albumin in blood can facilitate biomimetic delivery and deep tumor penetration. Efficient tumor accumulation and effective tumor suppression are successfully demonstrated with in vitro and in vivo studies. PTPE 1–3 salts exhibit dual functionality: they target and image mitochondria because of aggregation‐induced emission effects and they are promising for cancer therapy.