**Section 3 Mitochondrial Dysfunction and Neuronal Disorders 135**

Chapter 6 **Mitochondria at the Base of Neuronal Innate Immunity in Alzheimer's and Parkinson's Diseases 137** A. Raquel Esteves, Diana F. Silva, Daniel Santos, Emanuel Candeias, Filipa Filipe and Sandra M. Cardoso

Chapter 14 **Ethanol Consumption Affects Neuronal Function: Role of the**

Chapter 15 **Mitochondrial Oxidative Stress and Calcium-Dependent**

Chapter 16 **Ketamine Induces Neuroapoptosis in Stem Cell–Derived**

Chapter 17 **Modulation of Mitochondria During Viral Infections 443** Latif Reshi, Hao-Ven Wang and Jiann-Ruey Hong

**Section 7 Regulation of Structure and Function of Mitochondrion by**

Chapter 18 **Estrogen and Mitochondrial Function in Disease 463**

**Statins-Associated Side Effects 385**

de Oliveira and Anibal E. Vercesi

Zeljko J. Bosnjak and Xiaowen Bai

**Section 6 Viruses as Mitochondrial Modulators 441**

**Estrogen 461**

Cheril Tapia-Rojas, María José Pérez, Claudia Jara, Erick H. Vergara

Contents **VII**

**Permeability Transition are Key Players in the Mechanisms of**

Estela N.B. Busanello, Ana C. Marques, Estela Lorza-Gil, Helena C.F.

**Developing Human Neurons Possibly through Intracellular Calcium/Mitochondria/microRNA Signaling Pathway 421** Danielle Twaroski, Yasheng Yan, Congshan Jiang, Sarah Logan,

Ved P. Mooga, C. Roger White and Samantha Giordano-Mooga

**Mitochondria 361**

and Rodrigo A. Quintanilla


Chapter 8 **Mitochondrial Trafficking by Prohibitin-Kinesin-Myosin-Cadherin Complex in the Eye 209** Srinivas R. Sripathi, Weilue He, Johnpaul Offor, Diana R. Gutsaeva and Wan Jin Jahng

	- **Section 5 Chemicals as Mitochondrial Dysfunction Inducers 291**

Chapter 14 **Ethanol Consumption Affects Neuronal Function: Role of the Mitochondria 361**

**Section 3 Mitochondrial Dysfunction and Neuronal Disorders 135**

Chapter 6 **Mitochondria at the Base of Neuronal Innate Immunity in Alzheimer's and Parkinson's Diseases 137**

**Section 4 Mitochondrial Components and Their Roles in Diseases 181**

Chapter 7 **Protein Kinases and Regulation of Mitochondrial Function in**

Chapter 8 **Mitochondrial Trafficking by Prohibitin-Kinesin-Myosin-**

Chapter 9 **18 kDa Translocator Protein in Mitochondria-Related**

Chapter 10 **Hereditary Disorders and Human Mutations of Iron-Sulfur**

Chapter 11 **Nuclear Encoded Mitochondrial Proteins in Metabolite**

Janka Vašková, Jozef Firment and Ladislav Vaško

**Section 5 Chemicals as Mitochondrial Dysfunction Inducers 291**

Chapter 12 **Pyrethroid Insecticides as the Mitochondrial Dysfunction**

Celal Guven, Yusuf Sevgiler and Eylem Taskin

Chapter 13 **Mitochondrial Dysfunction Associated with Doxorubicin 323** Celal Guven, Yusuf Sevgiler and Eylem Taskin

Abraham Weizman and Moshe Gavish

**Pathology: The Case of Traumatic Brain Injury 227**

Filipa Filipe and Sandra M. Cardoso

**Ischemia/Reperfusion Injury 183**

**Cadherin Complex in the Eye 209**

Grażyna Nowak

**VI** Contents

and Wan Jin Jahng

**Assembly Genes 237**

Aldosary and Dilek Colak

**Nutrients 251**

**Inducers 293**

A. Raquel Esteves, Diana F. Silva, Daniel Santos, Emanuel Candeias,

Srinivas R. Sripathi, Weilue He, Johnpaul Offor, Diana R. Gutsaeva

Nahum Rosenberg, Nasra Yasin, Leo Veenman, Orit Rosenberg,

Namik Kaya, Zuhair Al-Hassnan, Maha Abdulrahim, Mazhor

**Transport and Oxidation Pathway Connecting Metabolism of**

Cheril Tapia-Rojas, María José Pérez, Claudia Jara, Erick H. Vergara and Rodrigo A. Quintanilla

Chapter 15 **Mitochondrial Oxidative Stress and Calcium-Dependent Permeability Transition are Key Players in the Mechanisms of Statins-Associated Side Effects 385**

Estela N.B. Busanello, Ana C. Marques, Estela Lorza-Gil, Helena C.F. de Oliveira and Anibal E. Vercesi


Preface

The cell has a dynamic and complex architecture; therefore, it is not in equilibrium with its environment. The environment constantly disrupts this dynamic and complex harmony. For cell maintenance, cells must absorb different types of energy from their environment and convert this energy into usable chemical forms. The mitochondrion plays a major role in supporting cellular homeostasis and formalizes the physiology of a cell as the most signifi‐ cant energy producer in aerobes. It also participates in cell death mechanisms. Therefore, mitochondrial dysfunction is implicated in the mode of action of many harmful factors for cells such as drugs and environmental contaminants, dysfunction of the oxygen transport

Multicellular organisms need oxygen to execute chemical transformations for ATP utiliza‐ tion and production as an energy transducer, and they need a pump for oxygen transport to the cells in hypoxic environments of their bodies. Heart function depends on continuous en‐ ergy supply, and therefore a complex mitochondrial network. Any factor affecting the mito‐ chondrial network will produce heart-related diseases and heart failure. Dr Stoll et al. tried to explain the role and the mechanism of mitochondria in the development of heart disease, and the progress in clinical diagnosis and treatments on a mitochondrial basis in recent studies. They proposed that further studies are required to confirm the effectiveness and toxicity of metabolic-modulating drugs and mitochondria-targeting antioxidants. As ex‐ plained in this chapter, changes in substrate utilization mechanisms should be solved for further understanding in developing effective treatment strategies against heart failure. Drs Bruns and Walker focused on the mechanism of right ventricular failure, which is less com‐ mon than the left ventricle failure. Both are mitochondria-related pathologies. A detailed ex‐ planation of the embryological, physiological, and pathophysiological differences between left and right ventricles is presented in their chapter in the view of recent studies. They re‐ ported that there is no right ventricle failure-targeted therapy and the current approach is extrapolating the therapeutic interventions for the left ventricular failure to the right one. However, there are some recent considerations to develop an effective therapy for right ven‐ tricle failure with further evaluations. Mitochondria accumulate the damaged and/or modi‐ fied proteins and mitochondrial DNA (mtDNA) during their life cycles. Mitophagy is an important physiological component for mitochondrial turnover to eliminate damaged or dysfunctional mitochondria to prevent further risk to the cell, especially to avoid unregulat‐ ed reactive oxygen formation. The healthy heart needs a fine balance between mitophagy and mitochondriogenesis; however, accumulation of damaged proteins and altered proteo‐ stasis in mitochondria is an important factor in age-related diseases of the heart. Dr Tatarko‐ va et al. have detailed the current knowledge on the physiological and biochemical changes in the mitochondrial functioning of the aging heart. They proposed that the development of

system, malnutrition, intense exercise, and genetic variations.
