Cellular Senescence 2025

npj Aging is edited by a team of external academic editors. 

Nature Aging is edited by a team of full-time professional editors.

Nature Metabolism is edited by a team of full-time prpfessional editors.

Nature Cell Biology is edited by a team of full-time professional editors.

Scientific Reports is managed by in-house professional editors and edited by Editorial Board Members.  

Guest Editors for npj Aging:

Diana Jurk, PhD, Mayo Clinic, United States

Diana Jurk is an Associate Professor of Physiology at Mayo Clinic. Her research investigates the molecular and cellular mechanisms underlying aging and age-related disorders that arise from cellular dysfunction. These studies span age-related neurodegeneration, including dementia, and obesity-associated conditions such as metabolic dysfunction associated fatty liver disease (MAFLD) and type 2 diabetes. A central focus of her work is understanding senescence pathways and how senescent cells communicate with their environment, influence neighboring and distant tissues, and shape systemic inflammation. By dissecting these cell-to-cell communication networks and tissue crosstalk, her research aims to identify new key players and therapeutic targets that improve healthspan.

J. Cesar Cardenas, PhD, Universidad Mayor, Chile

Over the past fifteen years, my academic journey has focused on unraveling the intricate role of calcium signaling mediated by the inositol 1,4,5-trisphosphate receptor (IP3R) in a broad range of cellular processes—including transcription, proliferation, autophagy, bioenergetics, and metabolism. My research has pioneered the concept that small, constitutive IP3R-mediated calcium releases, even in unstimulated conditions, are critical for cellular homeostasis. These localized signals are efficiently taken up by mitochondria and are indispensable for maintaining mitochondrial function and energy production across diverse cell types. Inhibition of this subtle yet essential calcium transfer induces energetic stress and activates autophagy as a compensatory, pro-survival mechanism. This calcium communication between the endoplasmic reticulum (ER) and mitochondria has emerged as a key regulator of both cancer cell homeostasis and, more recently, cellular senescence. Senescent cells, while physiologically beneficial during development and tissue repair, become detrimental when they accumulate—such as during aging or in response to chemo- or radiotherapy. Excessive senescent cell burden impairs tissue regeneration, contributes to frailty, and has been implicated in multiple age-related diseases. Moreover, senescent cells can promote tumorigenesis and cancer relapse through mechanisms that remain poorly understood. Therefore, identifying ways to delay senescence accumulation or eliminate senescent cells represents a promising therapeutic avenue. Understanding the signaling pathways that govern senescence, particularly those involving ER-mitochondrial calcium dynamics, is now a central focus of my work. My current research investigates how these inter-organelle calcium signals influence the initiation, establishment, and potential reversal of senescence, particularly in the context of cancer. Intriguingly, we have found that senescent cancer cells can acquire stem-like properties and escape the senescent state—a process in which ER-mitochondrial calcium transfer appears to play a pivotal role. The mechanistic basis of this phenomenon remains largely unexplored, and my lab is actively working to dissect it in detail.