Most energy required to drive metabolic activities inside a cell is produced by mitochondria, membrane-bound cell organelles (mitochondrion, singular). Adenosine triphosphate (ATP) is a small molecule that stores chemical energy generated by the mitochondria. Because of their tiny size (often between 0.75 and 3 micrometers), mitochondria must be dyed before being seen under the microscope. They have exterior and inner membranes, differentiating them from most other organelles (cellular mini-organs). Different membranes serve various purposes. Each section or compartment inside a mitochondria plays a specific function.
The quantity of mitochondria in a cell varies depending on its cell type. Mature red blood cells, for example, contain zero mitochondria, but liver cells might have over 2,000. More mitochondria are present in cells that need a lot of power. In cardiac muscle cells, mitochondria occupy around 40% of the cytoplasm.
Mitochondria are shown in textbooks as an oval, but they are continually fissioning and fusing. Therefore, in actuality, these organelles are connected in dynamic networks. Mitochondria, which are coiled in sperm cells' midpieces and provide energy for tail motion, are another example.
Mitochondria and Aging
Mitochondrial function declines due to age-related changes. The accumulation of mutations and oxidative damage brought on by reactive oxygen species (ROS) causes mitochondrial DNA to shrink in size, integrity, and function with age.
Several mitochondrial functions decline with age, including oxidative capability, oxidative phosphorylation, ATP synthesis, reactive oxygen species (ROS) formation, and antioxidant defense. Alterations in mitochondrial dynamics and suppression of mitophagy, an autophagy process that eliminates malfunctioning mitochondria, reduce mitochondrial biogenesis with age.
Mitochondrial quality control changes due to aging further compromise mitochondrial function. The fraction of apoptotic cells is higher in older tissues due in part to increased mitochondria-mediated apoptosis. Peptides have been actively researched to explore their potential in slowing mitochondrial aging and possibly mitigataing the age-related phenotype in animals.
SS-31 Peptide
Studies suggest that to protect the mitochondria from damage, one family of short peptides known as SS-31 may preferentially localize to the inner mitochondrial membrane. Research suggests that SS-31 (also known as MTP-131) is a mitochondria-targeting peptide that may be dissolved in water and is suggested to reduce the generation of reactive oxygen species and the secretion of cytochrome c in the mitochondria. Data suggests that this peptide may reverse the deterioration in diabetes, reduce the pulmonary arterial hypertension and heart failure brought on by transverse aortic constriction, and potentially revitalize oxidative phosphorylation as indicated by research findings in elderly animals.
MOTS-c Peptide
MOTS-c is a peptide generated from mitochondria, researched for its potential research applications, including fat storage reduction and increase in lean muscle growth, and reversal of cellular senescence. Interestingly, Asiatic studies have suggested phenotypic expression and biological relationship between MOTS-c and a longer life expectancy.
Investigations purport that increased mitochondrial biogenesis may result from the potential of MOTS-c to activate the mitochondrial genome. Studies suggest that murine synthesis and elevated PCG-1 alpha and AICAR may be induced by inhibiting the methionine-folate cycle; these molecules are considered to be critical to energy metabolism through AMP-activated protein kinase (AMPK). Cellular senescence may be partially prevented by activating AMPK.
Cellular Senescence: What is it?
Cells can halt when they detect injury. Cellular senescence, also known as cellular arrest, describes this phenomenon. Cells do this because they cannot increase when damage is present. They instead stop moving until the immune system eliminates them. Senescent cells continue to release harmful signals until they are eliminated. These signals accelerate aging by increasing inflammation and stem cell exhaustion.
MOTS-c, a peptide generated from mitochondria, has been hypothesized to help sustain metabolism and lower fat storage and insulin resistance.
While mitochondria's function as an organelle is widely considered to be understood, its value as a signaling unit is only now becoming recognized. Humanin, a signaling peptide, was recently discovered to be encoded by a short open reading frame (sORF) in the mitochondrial DNA (mtDNA). This raises the possibility that other sORFs might exist in the mtDNA. Here, researchers provide speculation that a small open reading frame (sORF) inside mitochondrial 12S rRNA may encode a peptide of 16 amino acids called MOTS-c (mitochondrial open-reading frame of the twelve S rRNA -c) that controls insulin sensitivity and metabolic balance. Its biological effects block the folate cycle and its linked de novo purine production, ultimately activating AMPK. Skeletal muscle seems to be its major target organ. Mice given MOTS-c appeared to be somewhat protected against weight gain and insulin resistance induced by a high-fat diet and advancing age. These findings suggest that mitochondria may actively use peptides encoded by their genome to control metabolic balance at the cellular and organismal levels.
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