Hiroshi Abe
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Hiroshi Abe has a total of 35 co-authors. Here are the top co-authors by number of shared publications:
- Fumitaka Kawakami
Regenerative Medicine and Cell Design Research Facility, School of Allied Health Sciences, Kitasato University, 1-15-1 Kitasato, Sagamihara 252-0373, Japan
2 shared publications - Hideyuki J. Majima
School of Allied Health Sciences, Walailak University, Nakhon Si Thammarat 80160, Thailand
2 shared publications - Hiroko P. Indo
Department of Oncology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima 890-8544, Japan
2 shared publications - Hiroshi Ichikawa
Department of Medical Life Systems, Graduate School of Life and Medical Sciences, Doshishia University, Kyoto 610-0394, Japan
2 shared publications Hisashi J. Beppu
Dr. Beppu’s Oral Health Care & Anti-Aging Clinic, Iwakami Building 3F, 3-2-6 Nihonbashi, Chuo-ku, Tokyo 103-0027, Japan
2 shared publications- Ikuo Nakanishi
Quantum RedOx Chemistry Team, Quantum Life Spin Group, Institute for Quantum Life Science (iQLS), National Institutes for Quantum Science and Technology (QST), Chiba-shi 263-8555, Chiba, Japan
2 shared publications
Latest Publications
- Open Access
HSP47 in Mitochondria: Roles in Apoptosis, Signal Transduction, and Protein and Virus Transportation
Mitochondria are essential organelles for cellular energy production and the regulation of diverse biological processes, including apoptosis, redox homeostasis, and intracellular signaling. Although mitochondrial reactive oxygen species (mtROS) act as critical mediators of these functions, the molecular mechanisms underlying mtROS regulation remain poorly understood. This review summarizes current insights into the role of heat shock protein 47 (HSP47) in mitochondrial oxidative stress and mtROS-mediated cellular responses. In addition to its classical function as an endoplasmic reticulum (ER) chaperone, HSP47 translocates to the mitochondria under oxidative stress conditions. This mitochondrial localization promotes mtROS production, thereby triggering apoptotic pathways and redox-sensitive signal transduction. Furthermore, we examine the mechanistic insights linking HSP47 to mitochondrial function and oxidative stress, highlighting their implications for cellular homeostasis and disease pathogenesis. Overall, these findings establish HSP47 as a novel regulator of mtROS generation, suggesting that the HSP47–mtROS axis represents a promising therapeutic target for oxidative stress-related disorders and a potential role for exploring virus-induced cellular responses in future research.
Open AccessHSP47 in Mitochondria: Roles in Apoptosis, Signal Transduction, and Protein and Virus Transportation
Mitochondria are essential organelles for cellular energy production and the regulation of diverse biological processes, including apoptosis, redox homeostasis, and intracellular signaling. Although mitochondrial reactive oxygen species (mtROS) act as critical mediators of these functions, the molecular mechanisms underlying mtROS regulation remain poorly understood. This review summarizes current insights into the role of heat shock protein 47 (HSP47) in mitochondrial oxidative stress and mtROS-mediated cellular responses. In addition to its classical function as an endoplasmic reticulum (ER) chaperone, HSP47 translocates to the mitochondria under oxidative stress conditions. This mitochondrial localization promotes mtROS production, thereby triggering apoptotic pathways and redox-sensitive signal transduction. Furthermore, we examine the mechanistic insights linking HSP47 to mitochondrial function and oxidative stress, highlighting their implications for cellular homeostasis and disease pathogenesis. Overall, these findings establish HSP47 as a novel regulator of mtROS generation, suggesting that the HSP47–mtROS axis represents a promising therapeutic target for oxidative stress-related disorders and a potential role for exploring virus-induced cellular responses in future research.
- Open Access
- 17 October 2024
- Published by MDPI AG in Biomolecules
- Vol. 14 (10) , 1317
The Roles of Mitochondria in Human Being’s Life and Aging
The universe began 13.8 billion years ago, and Earth was born 4.6 billion years ago. Early traces of life were found as soon as 4.1 billion years ago; then, ~200,000 years ago, the human being was born. The evolution of life on earth was to become individual rather than cellular life. The birth of mitochondria made this possible to be the individual life. Since then, individuals have had a limited time of life. It was 1.4 billion years ago that a bacterial cell began living inside an archaeal host cell, a form of endosymbiosis that is the development of eukaryotic cells, which contain a nucleus and other membrane-bound compartments. The bacterium started to provide its host cell with additional energy, and the interaction eventually resulted in a eukaryotic cell, with both archaeal (the host cell) and bacterial (mitochondrial) origins still having genomes. The cells survived high concentrations of oxygen producing more energy inside the cell. Further, the roles of mitochondria in human being’s life and aging will be discussed.
- 17 October 2024
- Published by MDPI AG in Biomolecules
- Vol. 14 (10) , 1317
Open AccessThe Roles of Mitochondria in Human Being’s Life and Aging
The universe began 13.8 billion years ago, and Earth was born 4.6 billion years ago. Early traces of life were found as soon as 4.1 billion years ago; then, ~200,000 years ago, the human being was born. The evolution of life on earth was to become individual rather than cellular life. The birth of mitochondria made this possible to be the individual life. Since then, individuals have had a limited time of life. It was 1.4 billion years ago that a bacterial cell began living inside an archaeal host cell, a form of endosymbiosis that is the development of eukaryotic cells, which contain a nucleus and other membrane-bound compartments. The bacterium started to provide its host cell with additional energy, and the interaction eventually resulted in a eukaryotic cell, with both archaeal (the host cell) and bacterial (mitochondrial) origins still having genomes. The cells survived high concentrations of oxygen producing more energy inside the cell. Further, the roles of mitochondria in human being’s life and aging will be discussed.