Mitochondrial Dysfunction in Ageing and Diseases / / edited by Jaime M. Ross, Giuseppe Coppotelli and Lars Olson.

• TeilnehmendeR: Ross, Jaime M.,; Coppotelli, Giuseppe,; Olson, Lars,
• Place / Publishing House: Basel : : MDPI,, 2016.; ©2016
• Year of Publication: 2016
• Language: English
• Physical Description: 1 online resource (xxvi, 516 pages) :; illustrations

The past decade has witnessed an explosion of knowledge regarding how mitochondrial dysfunction may translate into ageing and disease phenotypes, as well as how it is modulated by genetic and lifestyle factors. Impairment of the mitochondria may be caused by mutations or deletions in nuclear or mitochondrial DNA. Hallmarks of mitochondrial dysfunction include decreased ATP production, decreased mitochondrial membrane potential, swollen mitochondria, damaged cristae, increased oxidative stress, and decreased mitochondrial DNA copy number. In addition to energy production, mitochondria play an important role in regulating apoptosis, buffering calcium release, retrograde signaling to the nuclear genome, producing reactive oxygen species (ROS), participating in steroid synthesis, signaling to the immune system, as well as controlling the cell cycle and cell growth. Dysfunctional mitochondria have been implicated in ageing and in several diseases, many of which are age-related, including mitochondrial diseases, cancers, metabolic diseases and diabetes, inflammatory conditions, neuropathy, and neurodegenerative diseases such as Alzheimer's, Parkinson's, and Huntington's disease. Additionally, a possible link between mitochondrial metabolism and the ubiquitin-proteasome and autophagy-lysosome systems is emerging as a novel factor contributing to the progression of several human diseases. This special issue calls for original research, mini and full reviews, and perspectives that address the progress and current standing in the vast field of mitochondrial biology. These include, but are not limited to: ageing neurodegenerative diseases mitochondrial diseases metabolic diseases protein homeostasis cell/retrograde signaling oxidative stress pain cancer immune system therapies to counteract mitochondrial dysfunction.

Table of Contents

Giuseppe Coppotelli and Jaime M. Ross -- Naghia Ahmed, Dario Ronchi and Giacomo Pietro Comi -- Thierry Arnould, Sébastien Michel and Patricia Renard -- Lin Ding and Yilun Liu -- Jaime M. Ross, Lars Olson and Giuseppe Coppotelli -- Raffaella Crescenzo, Francesca Bianco, Arianna Mazzoli, Antonia Giacco, Giovanna Liverini and Susanna Iossa -- Paola Maura Tricarico, Sergio Crovella and Fulvio Celsi -- Jieying Zhang, Kunlu Wu, Xiaojuan Xiao, Jiling Liao, Qikang Hu, Huiyong Chen, Jing Liu and Xiuli An -- Yuliya Mikhed, Andreas Daiber and Sebastian Steven -- Janina A. Vaitkus, Jared S. Farrar and Francesco S. Celi -- Francesca Forini, Nadia Ucciferri, Claudia Kusmic, Giuseppina Nicolini,Antonella Cecchettini, Silvia Rocchiccioli, Lorenzo Citti and Giorgio Iervasi -- Francesca Forini, Giuseppina Nicolini and Giorgio Iervasi -- María Cecilia Cimolai, Silvia Alvarez, Christoph Bode and Heiko Bugger -- Ana A. Baburamani, Chloe Hurling, Helen Stolp, Kristina Sobotka,Pierre Gressens, Henrik Hagberg and Claire Thornton -- Yu Luo, Alan Hoffer, Barry Hoffer and Xin Qi -- Seok-Jo Kim, Paul Cheresh, Renea P. Jablonski, David B. Williams and David W. Kamp -- Giovanni Pagano, Annarita Aiello Talamanca, Giuseppe Castello, Mario D. Cordero, Marco d'Ischia, Maria Nicola Gadaleta, Federico V. Pallardó, Sandra Petrović, Luca Tiano and Adriana Zatterale -- Josephine S. Modica-Napolitano and Volkmar Weissig -- Xiaonan Zhang, Angelo de Milito, Maria Hägg Olofsson, Joachim Gullbo, Padraig D'Arcy and Stig Linder -- Kimitoshi Kohno, Ke-Yong Wang, Mayu Takahashi, Tomoko Kurita, Yoichiro Yoshida, Masakazu Hirakawa, Yoshikazu Harada, Akihiro Kuma, Hiroto Izumi and Shinji Matsumoto -- Zhicheng Wang, Jie Wang, Rufeng Xie, Ruilai Liu and Yuan Lu -- Ruey-Sheng Wang, Heng-Yu Chang, Shu-Huei Kao, Cheng-Heng Kao, Yi-Chen Wu, Shuyuan Yeh, Chii-Reuy Tzeng and Chawnshang Chang.