Core Viewpoint - The research published by Professor Yang Chonglin's team from Yunnan University reveals that the mitochondria-associated condensates (MATO) formed by the RNA-binding protein LARP-1 through liquid-liquid phase separation (LLPS) play a crucial role in maintaining mitochondrial homeostasis and promoting lifespan extension [3][5]. Group 1 - The study demonstrates that MATO mediates the local synthesis of proteins necessary for maintaining mitochondrial structure and function [5]. - In Caenorhabditis elegans, LARP-1 coordinates the translation mechanism and the fusion of various RNA-binding proteins to form MATO, which is dependent on the mitochondrial outer membrane complex transport enzyme [5]. - A deficiency in LARP-1 significantly reduces mitochondrial protein levels, disrupts the organization of mitochondrial cristae, and affects ATP production [5]. Group 2 - The research identifies that the synthesis of MICOS subunit IMMT-1 (MIC60) and ATP synthase β subunit ATP-2, which are critical for mitochondrial cristae organization, is decreased in LARP-1 deficient worms [5]. - During aging and starvation, LARP-1 MATO dissociates from the mitochondria; however, its persistent presence in mitochondria can protect mitochondrial health and greatly extend lifespan [5][7].

Core Viewpoint - The article discusses the development of a nanomedicine (EM-eNM) that engages energy metabolism to maintain mitochondrial homeostasis, alleviate cellular aging, and reverse age-related diseases [4][10]. Group 1: Research Background - Mesenchymal stem cells (MSC) play a crucial role in maintaining balance and promoting tissue repair, but aging impairs their function and regenerative capacity, leading to age-related diseases like osteoporosis [2]. - Mitochondrial dysfunction is a significant feature of aging MSC, characterized by mitochondrial homeostasis disruption, including impaired mitophagy and accumulation of dysfunctional mitochondria [2][9]. Group 2: Nanomedicine Development - The research team developed EM-eNM based on the structure and function of ATP synthase, a key enzyme in energy generation, to restore vitality in aging MSC and prevent skeletal aging [7]. - EM-eNM can penetrate the mitochondria of aging bone marrow MSC, promoting mitochondrial fission, mitophagy, and glycolysis, thereby maintaining the stemness and pluripotency of BMMSC [9]. Group 3: Therapeutic Potential - Systemic administration of EM-eNM via tail vein injection selectively targets bone tissue, significantly reversing osteoporosis-related bone loss in aged mice while restoring the stemness and osteogenic potential of BMMSC in situ [9]. - The study highlights the potential of EM-eNM as a targeted therapy for alleviating cellular aging and age-related diseases [10].