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What Is The Role Of Mitochondria In Plants

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Gene Introduction Into The Mitochondria Of Arabidopsis Thaliana Via Peptide Based Carriers

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By Xiaoqin Zhang Xiaoqin Zhang Scilit Preprints.org Google Scholar 1, 2, 3 , Ewud Agborbesong Ewud Agborbesong Scilit Preprints.org Google Scholar 1, 3, 4 and Xiaogang Li Xiaogang Li Scilit Preprints.org Google Scholar 1, 3, *

Received: 13 September 2021 / Revised: 10 October 2021 / Accepted: 13 October 2021 / Published: 19 October 2021

The Mystery Of Massive Mitochondrial Complexes: The Apicomplexan Respiratory Chain: Trends In Parasitology

Mitochondria are heterogeneous and highly dynamic organelles, playing a key role in adenosine triphosphate (ATP) synthesis, metabolic processing, oxygen species (ROS) production, and cell differentiation and death. Mitochondrial dysfunction is known to be a contributor to many diseases. The kidney is an organ rich in mitochondria and requires a lot of energy in the human body. Recent studies have focused on the role of mitochondrial dysfunction in the pathogenesis of various kidney diseases, including acute kidney injury (AKI) and chronic kidney disease (CKD). ). AKI is associated with an increased risk of CKD. AKI and CKD have a wide clinical morbidity and a significant impact on morbidity and mortality, which include various etiologies and represent a major public health challenge worldwide. structure, dynamics, and biogenesis as well as the crosstalk of mitochondria with other organelles. Chronic dysregulation of mitochondrial homeostasis in AKI and CKD affects various cellular pathways, leading to increased renal microvascular loss, oxidative stress, apoptosis, and kidney failure. It is important to understand the cellular and molecular events that control mitochondrial function and the pathophysiology of AKI and CKD, which should facilitate the development of new therapeutic strategies. This review provides an overview of the molecular insights of mitochondria and the specific pathogenic mechanisms of mitochondrial dysfunction in AKI, CKD, and the progression of AKI to CKD. We discuss the potential benefits of mitochondrial therapies in the treatment of mitochondrial dysfunction-mediated AKI and CKD, which may translate into therapeutic options to improve kidney injury and delay the progression of these kidney disease.

Acute kidney injury (AKI), formerly known as renal failure, is defined as sudden kidney failure, ranging from mild loss of kidney function to complete failure of the kidney. seeds and can occur within a few hours or days [1]. AKI can affect other organs such as the brain, heart and lungs and is associated with significant morbidity [2]. The causes of AKI in addition to reduced blood flow, include direct damage to the kidney and blockage of blood vessels [3]. Chronic kidney disease (CKD) is defined as the presence of persistent kidney damage over a long period of time, such as three months or more. CKD can cause waste in your body and can cause other health problems as well. The causes of CKD vary worldwide, and may include diabetes, hypertension, primary glomerulonephritis, chronic tubulointerstitial nephritis, hereditary or cystic diseases, heart disease, and stroke [ 4 , 5 ]. Although AKI and CKD were previously considered to be two separate syndromes, it is now known that they are closely related or an interconnected syndrome, because AKI is one of the main factors that accelerate the development of CKD [6], and CKD causes or notices. patients with AKI [7]. Research suggests that incomplete or maladaptive repair after AKI leads to tubulointerstitial fibrosis and ultimately to CKD [ 8 , 9 ]. The transition between AKI and CKD represents a global health challenge [10]. Currently, the treatment of AKI and CKD is based on targeting the underlying cause rather than a proven specific treatment. Therefore, understanding the molecular mechanisms underlying AKI and CKD is important for drug development and the generation of new therapeutic strategies for these kidney diseases.

The kidney is one of the most energy-demanding organs in humans and has the highest mitochondrial content and oxygen consumption after the heart. Mitochondria is a network of plastic organelles that can produce adenosine triphosphate (ATP), thus providing the energy for the basal cell function in the kidney [11, 12]. Mitochondria play an important role in metabolic processes, production of reactive oxygen species, maintenance of intracellular calcium homeostasis, thermogenesis, and regulation of proliferation and intrinsic apoptotic pathways [13, 14]. Mitochondrial populations can differ in size, mass, metabolic activity, and membrane potential within cells. Different nephron segments have different densities and distributions of mitochondria due to different energy requirements. Renal proximal tubular cells require high energy for reabsorption and secretion against chemical gradients. Proximal tubular cells generate ATP mainly through mitochondrial oxidative phosphorylation, whereas podocytes and endothelial and mesangial cells show more flexibility in their glycolytic capacity to produce energy [ 15 , 16 ]. Accumulating evidence indicates that various lethal and chronic injuries can lead to mitochondrial respiratory oxidative stress, ultrastructural defects, abnormal activation of the mitochondrial apoptosis pathway, DNA unstable mitochondrial (mtDNA), and the purification of damaged mitochondria. Mitochondrial dysfunction may increase the risk of tubular interstitial disease, cystic kidney disease, podocytopathy, and nephrotic syndromes [11]. Therefore, it is important for us to understand the mitochondrial biology and pathophysiology of AKI and CKD. A better understanding of the cellular and molecular events that regulate mitochondrial function in kidney disease should facilitate the development of therapeutic strategies. This review provides an overview of the molecular insights into the role of mitochondria in the development of AKI, CKD, and the transition from AKI to CKD.

The term AKI was first used by William MacNider in 1918 in the context of acute microbial poisoning and has recently been used to replace the term acute renal failure (ARF) [17]. AKI is a widespread clinical disease that rarely has a unique and unique pathophysiology, with an incidence of about 2000 per million population. Patients with AKI often have a mixed etiology, including specific kidney disease (eg, acute interstitial nephritis, acute glomerular and vasculitic renal disease); unspecified conditions (eg, ischemia, toxic injury); as well as extrarenal pathology (eg, prerenal azotemia and acute postrenal obstructive nephropathy) [1, 18]. The current diagnostic method of AKI is based on a short-term decrease in glomerular filtration rate (GFR), which is also reflected in an increase in serum creatinine and/or or decreased urine output [17, 19] .

Plant Cell Diagram, Structure, Types And Functions

AKI can be classified into three main categories: pre-renal, intrinsic, and post-renal AKI [3, 20]. Pre-renal and post-renal AKI are caused by a decrease in GFR in additional diseases, whereas ‘intrinsic’ AKI represents true kidney disease. AKI is characterized by impaired renal hemodynamics, renal tubular damage, renal congestion, and inflammation [21]. The pathogenesis of AKI involves the injury and death of renal tubular cells in the proximal tubule [ 21 , 22 ]. In AKI, the primary site of damage is the plasma membrane, but other cellular components, including the nucleus, cytoskeleton, endoplasmic reticulum (ER), and mitochondria, are major targets [ 22 ]. A variety of patient-specific factors and conditions may increase the risk of AKI, which can be classified as non-modifiable and modifiable factors, including advanced age, proteinuria, disease comorbid, anemia, severe disease, sepsis, and fluid overload [23].

CKD is characterized by gradual loss of kidney function over time and is defined as an eGFR <60 mL/min/1.73 m.

, regardless of the presence or absence of renal impairment, and includes stage 3 CKD (eGFR = 30–59 mL/min/1.73 m

Or people on chronic dialysis), which is also called end-stage renal disease (ESRD). ESRD is defined as end-stage chronic kidney disease, in which kidney function has declined to the point where the kidney can no longer function on its own [24]. In addition to the risk of progression to ESRD, CKD may be an independent cause of cardiovascular morbidity and mortality. The pathological features of CKD including the renal system and

Do Mitochondria Need Energy To Make Energy?

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