arXiv subjects

Jicun Wang-Michelitsch

Publications and source records attributed to Jicun Wang-Michelitsch.

17 recordsLinked to original sources

arXiv2018

Potential of longevity: hidden in structural complexity

In order to understand the phenomenon of longevity in biological world, the relationship between the potential of longevity and the structural complexity of an organism is analyzed. I. The potential of longevity is the maximum lifespan of an organism if it lives in an ideal environment. The longevity of an organism includes two parts: the time for development (development time) and the time for structure-maintenance (maintenance time). II. The development time of an organism depends on its structural complexity. The maintenance time is related to two factors: the degree of damage-exposure and the potential of functionality for structure-maintenance. The potential of functionality is built in structural complexity. Since both of development time and maintenance time are determined by structural complexity, the potential of longevity of an organism is hidden in structural complexity. III. The individuals of different species have different potentials of longevity because they have different structural complexities. An animal has limited longevity because it has limited structural complexity. Limited structural complexity and limited longevity are essential for the survival of a species. IV. Despite having the same potential of longevity, the individuals of a species can have different lifespans. The lifespan of an individual is more related to the degree of damage-exposure, which is determined by the living environment and the living habit of the individual. In conclusion, the potential of longevity of an organism is hidden in structural complexity, but the real lifespan of an organism is more related to the living environment.

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arXiv2018

Acute lymphoblastic leukemia may develop as a result of rapid transformation of a lymphoblast triggered by repeated bone-remodeling during bone-growth

Acute lymphoblastic leukemia (ALL) and chronic lymphocytic leukemia (CLL) are two major forms of leukemia that arise from lymphoid cells (LCs). ALL occurs mostly in children and CLL occurs mainly in old people. However, the Philadelphia-chromosome-positive ALL (Ph+-ALL) and the Ph-like ALL occur in both children and adults. To understand childhood leukemia/lymphoma, we have recently proposed two hypotheses on the causes and the mechanism of cell transformation of a LC. Hypothesis A is: repeated bone-remodeling during bone-growth and bone-repair may be a source of cell injuries of marrow cells including hematopoietic stem cells (HSCs), myeloid cells, and LCs. Hypothesis B is: a LC may have three pathways on transformation: a slow, a rapid, and an accelerated. We discuss in the present paper the developing mechanisms of ALL and CLL by these hypotheses. Having a peak incidence in young children, ALL may develop mainly as a result of rapid cell transformation of a lymphoblast (or pro-lymphocyte). Differently, Ph+-ALL and Ph-like ALL may develop as results of transformation of a lymphoblast via accelerated pathway. Occurring mainly in adults, CLL may be a result of transformation of a memory B-cell via slow pathway. By causing cell injuries of HSCs and LCs, repeated bone-remodeling during bone-growth and bone-repair may be related to the cell transformation of a LC. In conclusion, ALL may develop as a result of cell transformation of a lymphoblast via rapid or accelerated pathway; and repeated bone-remodeling during bone-growth may be a trigger for the cell transformation of a lymphoblast in a child.

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arXiv2018

Pediatric lymphoma may develop by "one-step" cell transformation of a lymphoid cell

Lymphomas are a large group of neoplasms developed from lymphoid cells (LCs) in lymph nodes (LNs) or lymphoid tissues (LTs). Some forms of lymphomas, including Burkitt lymphoma (BL), ALK+ anaplastic large cell lymphoma (ALK+-ALCL), and T-cell lymphoblastic lymphoma/leukemia (T-LBL), occur mainly in children and teenagers. Hodgkin's lymphoma (HL) has a peak incidence at age 20s. To understand pediatric lymphoma, we have recently proposed two hypotheses on the causes and the mechanism of cell transformation of a LC. Hypothesis A is: repeated bone-remodeling during bone-growth and bone-repair may be a source of cell injuries of marrow cells including hematopoietic stem cells (HSCs), myeloid cells, and LCs, and thymic involution may be a source of damage to the developing T-cells in thymus. Hypothesis B is: a LC may have three pathways on transformation: a slow, a rapid, and an accelerated. In this paper, we discuss pediatric lymphomas by this hypothesis. Having a peak incidence at young age, BL, T-LBL, ALK+-ALCL, and HL develop more likely as a result of rapid transformation of a LC. In BL, ALK+-ALCL, and HL, the cell transformations may be triggered by severe viral infections. In T-LBL, the cell transformation may be related to thymic involution. Occurring in both adults and children, diffuse large B-cell lymphoma (DLBCL) may develop via slow or accelerated pathway. In conclusion, pediatric lymphoma may develop as a result of "one-step" cell transformation of a LC, and severe viral infections may be the main trigger for the rapid transformation of a LC in a LN/LT.

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arXiv2018

Development of pediatric myeloid leukemia may be related to the repeatedbone-remodeling during bone-growth

Acute myeloid leukemia (AML) and chronic myeloid leukemia (CML) are two major formsof leukemia developed from myeloid cells (MCs). To understand why AML and CML occurin children, we analyzed the causes and the mechanism of cell transformation of a MC. I. Forthe MCs in marrow cavity, repeated bone-remodeling during bone-growth may be a source ofcell injuries. II. As a type of blood cell, a MC may have higher survivability from DNAchanges and require obtaining fewer cancerous properties for cell transformation than a tissuecell. III. Point DNA mutations (PDMs) and chromosome changes (CCs) are the two majortypes of DNA changes. CCs have three subtypes by effects on a cell: great effect CCs(GECCs), mild-effect CCs (MECCs), and intermediate-effect CCs (IECCs). A GECC affectsone or more genes and can alone trigger cell transformation. PDMs/MECCs are mostly mildand can accumulate in cells. Some of the PDMs/MECCs contribute to cell transformation. AnIECC affects one or more genes and participates in cell transformation. IV. Based on II andIII, we hypothesize that a MC may have two pathways on transformation: a slow and anaccelerated. Slow pathway is driven by accumulation of PDMs/MECCs. Accelerated pathwayis driven by accumulation of PDMs/MECCs/IECC(s). A transformation via slow pathwayoccurs at old age; whereas that via accelerated pathway occurs at any age. Thus, CML andpediatric AML may develop via accelerated pathway, and adult AML may develop via bothpathways. In conclusion, pediatric AML and CML may develop as a result of transformationof a MC via accelerated pathway; and repeated bone-remodeling for bone-growth may be atrigger for the transformation of a MC in a child.

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arXiv2018

Three pathways of cell transformation of lymphoid cell: a slow, a rapid, and an accelerated

Lymphoid leukemia (LL) and lymphoma are neoplasms developed from lymphoid cells (LCs). To understand why different forms of LL/lymphoma occur at different ages, we analyzed the effects of different types of DNA changes on a LC and the cellular characteristics of LCs. Point DNA mutations (PDMs) and chromosome changes (CCs) are the two major types of DNA changes. CCs have three subtypes by their effects on a LC: great-effect CCs (GECCs), mild-effect CCs (MECCs), and intermediate-effect CCs (IECCs). PDMs and MECCs are mostly mild thus can accumulate in cells. Some of the PDMs/MECCs contribute to cell transformation. A GECC affects one or more genes and can alone drive cell transformation. An IECC affects one or more genes and participates in cell transformation. Due to cellular characteristics, a LC may have higher survivability from DNA changes and require obtaining fewer cancerous properties for transformation than a tissue cell. Hence, a LC can be more rapidly transformed by a CC. On this basis, we hypothesize that a LC may have three pathways on transformation: a slow, a rapid, and an accelerated. Slow pathway is driven by accumulation of PDMs/MECCs. Rapid pathway is driven by a GECC in "one step". Accelerated pathway is driven by accumulation of PDMs/MECCs/IECC(s). Cell transformations of a LC via different pathways occur at different ages. A transformation via slow pathway occurs mainly in adults. A transformation via rapid pathway occurs at any age and has no increasing incidence with age. A transformation via accelerated pathway occurs also at any age but has increasing incidence with age. In conclusion, a LC may have three pathways on cell transformation, and the occurring age of LL/lymphoma may be determined by the transforming pathway of a LC.

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arXiv2018

Three potential sources of cell injuries of lymphoid cells associated with developments of lymphoid leukemia and lymphoma

Lymphoid leukemia (LL) and lymphoma are blood cancers developed from lymphoid cells (LCs). To understand the cause and the mechanism of cell transformation of a LC, we studied the potential sources of cell injuries of LCs and analyzed how DNA changes are generated and accumulate in LCs. I. The DNA changes that contribute to cell transformation of a LC can be generated in the LCs in marrow, thymus, lymph nodes (LNs), and/or lymphoid tissues (LTs). In LNs/LTs, pathogen-infections may be the main cause for cell injuries of LCs. In marrow cavity, repeated bone-remodeling during bone-growth and bone-repair, by producing toxic substances, may be a source of damage to hematopoietic cells, including hematopoietic stem cells (HSCs) and developing LCs. In thymus, thymic involution and death of stromal cells may be a damaging factor for the developing T-cells. II. Point DNA mutation (PDM) and chromosome change (CC) are the two major types of DNA changes. CCs include numerical CCs (NCCs) and structural CCs (SCCs). Generation of a PDM/SCC may be a result of Misrepair of DNA on DNA breaks. Generation of NCC is rather a consequence of dysfunction of cell division. III. Repeated cell injuries and cell proliferation drive the accumulation of DNA changes in LCs and HSCs. However, long-term accumulation of DNA changes occurs mainly in long-living stem cells including HSCs and memory cells. In conclusion, the DNA changes in LCs are generated and accumulate as a consequence of repeated cell injuries and repeated cell proliferation; and three potential sources of cell injuries of LCs may be: repeated bone-remodeling, long-term thymic involution, and repeated pathogen-infections.

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arXiv2018

Development of aging changes: self-accelerating and inhomogeneous

Aging changes including age spots and atherosclerotic plaques develop in an inhomogeneous and accelerated manner. For understanding this phenomenon, some aging changes are analyzed by Misrepair mechanism, a mechanism proposed in Misrepair-accumulation theory. I. Misrepair is a strategy of repair for survival of an organism in situations of severe injuries; however a Misrepair alters the structure of a tissue, a cell or a molecule, which are the sub-structures of an organism. II. Misrepair of a sub-structure also alters the spatial relationship of this sub-structure with its neighbor sub-structures. Thus a Misrepair leads to increased damage-sensitivity and reduced repair-efficiency of these sub-structures. As a result, Misrepairs have a tendency to occur to the sub-structure and its neighbor sub-structures where an old Misrepair has taken place. In return, new Misrepairs will increase again the damage-sensitivity of these sub-structures and the surrounding sub-structures. By such a vicious circle, the frequency of Misrepairs to these sub-structures is increased and the range of affected sub-structures is enlarged after each time of Misrepair. Thus, accumulation of Misrepairs is focalized and self-accelerating. III. Focalized accumulation of Misrepairs leads to formation and growing of a "spot" or "plaque" in a tissue. Growing of a spot is self-accelerating, and old spots grow faster than new ones. New spots tend to develop close to old ones, resulting in an inhomogeneous distribution of spots. In conclusion, the inhomogeneous development of aging changes is a result of self-accelerated and focalized accumulation of Misrepairs; and the process of aging is self-accelerating.

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arXiv2018

Development of age spots as a result of accumulation of aged cells in aged skin

Age spots are the brown spots that develop in the skin but change in color and shape with time. To understand the mechanism of development of age spots, characteristics of age spots are analyzed by Misrepair mechanism, a mechanism introduced in Misrepair-accumulation aging theory. An age spot is pathologically a group of aggregated basal cells, which contain lipofuscin bodies. Accumulation of lipofuscin bodies is a sign of aging of a cell. Characteristics of age spots include: inhomogeneity in distribution, growing flatly before becoming protruding, irregularity on shape, inhomogeneity on the color and on the protruding degree of a spot, and softness of a protruding spot. After analyzing these characteristics, we make a hypothesis on the process of development of an age spot. A. Aging of a tissue is the basis for development of age spots. B. A flat spot results from accumulation of lipofuscin containing cells. When an aged cell remains, this cell can accelerate the aging of its neighbor cells by increasing damage sensitivity and reducing repair efficiency of the local tissue. By a viscous circle, more and more neighbor cells become aged and they form a flat spot, which has an irregular shape. C. A protruding spot develops when some of the cells in a flat spot die and release lipofuscin bodies. For the survival of an organism, the un degradable lipofuscin bodies have to be isolated by a capsule made by fibrotic membrane, for maintaining the structural integrity of local epidermis. Successive deaths of lipofuscin containing cells make the capsule include more and more dead substances by layers of fibrotic membrane. In this way, the spot "grows" in three-dimension, resulting in protruding of the spot. In conclusion, development of an age spot is a result of accumulation of aged cells in aged skin.

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arXiv2018

The high osmotic pressure in a lens fiber as a driving force for the development of senile cortical cataract

In lens cataract, the clouding change in lens leads to a decline of transparency of part of the lens. There are three types of senile cataract: cortical cataract, nuclear cataract, and posterior/anterior sub-capsular cataract. The most common senile cataract is cortical cataract. For understanding cortical cataract, the pathology and the causing factors in cortical cataract are analyzed. The clouding change in senile cortical cataract begins from the edge of the lens and develops progressively to lens centre. The pathology of clouding change in cortical cataract is characterized by disruption of some lens fibers, swelling of some other fibers, and deposition of water between fibers. Based on the property of a lens fiber, we propose here a hypothesis on the mechanism of development of senile cortical cataract. I. Cortical cataract is triggered by disruption of a cortical lens fiber as a result of injury. The disrupted fiber will release water and crystallin proteins. II. Neighbor fibers can absorb this water due to high intracellular osmotic pressure (IOP) and become swollen. Swelling makes a fiber be stiff and have increased risk to disrupt when it is curved during the accommodation of the lens. These fibers will release water again when they disrupt, and the water will make more local fibers swelling. In this way, the local fibers become swollen and then disrupt successively. III. The successive swellings and disruptions of local fibers result in enlargement of a clouding change in lens. Since the fibers on the outer part of lens cortex have higher risk to be injured than that in the inner part, a clouding change starts from the edge of the lens. In conclusion, the progressive development of senile cortical cataract is a result of successive swellings and disruptions of local lens fibers, and this is driven by the high IOP in a lens fiber.

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arXiv2017

Misrepair mechanism in the development of atherosclerotic plaques

Atherosclerosis is a disease characterized by the development of atherosclerotic plaques (APs) in arterial endothelium. The APs in part of an arterial wall are inhomogeneous on size and on distribution. In order to understand this in-homogeneity, the pathology of APs is analyzed by Misrepair mechanism, a mechanism proposed in our Misrepair-accumulation aging theory. I. In general, development of an AP is a result of repair of injured endothelium. Because of infusion and deposition of lipids beneath endothelial cells, the repair has to be achieved by altered remodeling of local endothelium. Such a repair is a Misrepair. During repair, smooth muscular cells (SMCs) are clustered and collagen fibers are produced to the lesion of endothelium for reconstructing an anchoring structure for endothelial cells and for forming a barrier to isolate the lipids. II. Altered remodeling (Misrepair) makes the local part of endothelium have increased damage-sensitivity and reduced repair-efficiency. Thus, this part of endothelium will have increased risk for injuries, lipid-infusion, and Misrepairs. Focalized accumulation of Misrepairs and focalized deposition of lipids result in development of a plaque. III. By a viscous circle between lipid-infusion and endothelium-Misrepair, growing of an AP is self-accelerating. Namely, once an AP develops, it grows in an increasing rate with time and it does not stop growing. Within part of an arterial wall, older APs grow faster than younger ones. The oldest and the biggest AP is the most threatening one in narrowing local vessel lumen. Therefore, the self-accelerated growing of an AP is a fatal factor in atherosclerosis. In conclusion, development of APs is focalized and self-accelerating, because it is a result of accumulation of Misrepairs of endothelium.

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arXiv2017

Tissue fibrosis: a principal proof for the central role of Misrepair in aging

Tissue fibrosis is the phenomenon that a tissue has progressive deposition of collagen fibers with age. Tissue fibrosis is associated with aging of most of our organs, and it is the main pathology in arteriosclerosis, chronic bronchitis/emphysema, and benign prostatic hyperplasia. The causes and characteristics of fibrosis are analyzed with Misrepair mechanism, a mechanism proposed in Misrepair-accumulation aging theory. Tissue fibrosis is known to be a result of repairs of tissue by collagen fibers. A repair with collagen fibers is a manner of "Misrepair". The collagen fibers are used for replacing dead cells or disrupted extracellular matrixes (ECMs) including elastic fibers, myofibers, and basement membrane. The progressive tissue fibrosis with age manifests the essential role of Misrepair in aging, because it reveals three facts: A. a process of Misrepair exists; B. Misrepairs are unavoidable; and C. Misrepairs accumulate. As a result of accumulation of Misrepairs of tissue with collagen fibers, tissue fibrosis is focalized and self-accelerating, appearing as growing of spots of hyaline degeneration. Fibrosis results in stiffness or atrophy of an organ and progressive failure of the organ. In arteriosclerosis, the deposition of collagen fibers in arterial wall is for replacing disrupted elastic fibers or myofibers, however results in hardness of the wall. Wrinkle formation is part of skin fibrosis, and it may be a result of accumulation of collagen fibers of different lengths. Senile hair-loss and hair-whitening are probably consequence of dermal fibrosis. In conclusion, tissue fibrosis is a result of accumulation of Misrepairs of tissue with collagen fibers, and the phenomenon of fibrosis is a powerful proof for the central role of Misrepair in aging.

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arXiv2017

Premature aging as a consequence of Mis-construction of tissues and organs during body development

Hutchinson-Gilford Progeria syndrome, Werner syndrome, and Cockayne syndrome are three genetic disorders, in which the children have premature aging features. To understand the phenomenon of premature aging, the similarity of aging features in these syndromes to that in normal aging is investigated. Although these three syndromes have different genetic backgrounds, all the patients have abnormal structures of tissues/organs like that in normal aging. Therefore, the abnormality in tissue structure is the common point in premature aging and normal aging. This abnormality links also a defective development and a defective repair, the Misrepair. Defective development is a result of Mis-construction of the structure of tissues and organs as consequence of genetic mutations. Aging is a result of Mis-reconstructions, the Misrepairs, for maintaining the structure of tissues/organs. Construction-reconstruction of the structure of an organism is thus the coupling point of development and aging. Mis- construction and Mis-reconstruction (Misrepair) are the essential processes for the development of aging-like feathers. In conclusion, premature aging is a result of Mis- construction of tissues and organs during body development as consequence of genetic disorders.

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arXiv2017

Cell transformation in tumor-development: a result of accumulation of Misrepairs of DNA through many generations of cells

Development of a tumor is known to be a result of accumulation of DNA changes in somatic cells. However, the processes of how DNA changes are produced and how they accumulate in somatic cells are not clear. DNA changes include two types: point DNA mutations and chromosome changes. However, point DNA mutations (DNA mutations) are the main type of DNA changes that can remain and accumulate in cells. Severe DNA injuries are the causes for DNA mutations. However, Misrepair of DNA is an essential process for transforming a DNA injury into a survivable and inheritable DNA mutation. In somatic cells, Misrepair of DNA is the main source of DNA mutations. Since the surviving chance of a cell by Misrepair of DNA is low, accumulation of DNA mutations can take place only possibly in the cells that can proliferate. Tumors can only develop in the tissues that are regenerable. The accumulation of Misrepairs of DNA needs to proceed in many generations of cells, and cell transformation from a normal cell into a tumor cell is a slow and long process. However, once a cell is transformed especially when it is malignantly transformed, the deficiency of DNA repair and the rapid cell proliferation will accelerate the accumulation of DNA mutations. The process of accumulation of DNA mutations is actually the process of aging of a genome DNA. Repeated cell injuries and repeated cell regenerations are the two preconditions for tumor-development. For cancer prevention, a moderate and flexible living style is advised.

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arXiv2017

Misrepair mechanism: a mechanism essential for individual adaptation, species adaptation and species evolution

In Misrepair-accumulation theory, we have proposed a Misrepair mechanism for interpreting aging. However, Misrepair mechanism is also important in biological adaptation. Misrepair is a strategy of repair for increasing the surviving chance of an organism when it suffers from severe injuries. As a surviving strategy, Misrepair mechanism plays also an important role in individual adaptation, species survival, and species differentiation. Firstly, Misrepair of an injury is one of the manners of individual adaptation; and Misrepair mechanism gives an organism a great potential in adapting to changeable and destructive environment. Secondly, Misrepair mechanism is important in maintaining and enlarging the diversity of genome DNAs of a species; and a large diversity of genome DNAs is essential for the adaptation and the differentiation of a species in different environments. On one hand, somatic Misrepairs are essential for maintaining the sufficient number of individuals in a species, which are the vectors of different genome DNAs. On the other hand, Misrepair of DNA is a source of DNA mutations and the DNA Misrepairs in germ cells may contribute to the diversity of genome DNAs in a species. In conclusion, Misrepair mechanism is a mechanism essential for individual adaptation, species adaptation, and species evolution.

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arXiv2017

Misrepair accumulation theory: a theory for understanding aging, cancer development, longevity, and adaptation

Misrepair accumulation theory is a novel theory in interpreting aging phenomena. With a new concept of Misrepair, this theory reaches a unified understanding of aging: aging of an organism is a result of accumulation of Misrepairs of its structure. Misrepair accumulation theory (MA theory) is distinct and it can improve our understanding of life on several aspects. I. MA theory is fundamentally different from other theories by: A. proposing a generalized concept of Misrepair; B. pointing out the evolutionary advantage of aging mechanism; and C. distinguishing between aging of a cell and aging of a tissue. II. MA theory overcomes the limitations of traditional theories on interpreting the phenomena of tissue fibrosis and cancer development. Tissue fibrosis, as a result of accumulation of Misrepairs with collagen fibers, is a powerful evidence for demonstrating the central role of Misrepairs in aging. Cancer development is a result of accumulation of DNA Misrepairs in somatic cells, which needs to proceed over many generations of cells in a regenerable tissue. III. MA theory improves also our understanding on longevity, premature aging, adaptation, and species evolution. The potential of longevity of an organism is hidden in the complexity of its structure. IV. MA theory suggests that for retarding aging, the most important is to reduce the opportunity of damage-exposure.

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arXiv2017

Traditional aging theories: which ones are useful?

Many theories have been proposed to answer two questions on aging: "Why do we age?" and "How do we age?" Among them, evolutionary theories are proposed to interpret the evolutionary advantage of aging, and "saving resources for group benefit" is thought to be the purpose of aging. However for saving resources, a more economic strategy should be to make a rapid death to the individuals who are over the reproduction age rather than to make them aging. Biological theories are proposed to identify the causes and the biological processes of aging. However, some theories including cell senescence/telomere theory, gene-controlling theory, and developmental theory, have unfortunately ignored the influence of damage on aging. Free-radical theory suggests that free radicals by causing intrinsic damage are the main cause of aging. However, even if intracellular free radicals cause injuries, they could be only associated with some but not all of the aging changes. Damage (fault)-accumulation theory predicts that faults as intrinsic damage can accumulate and lead to aging. However, in fact an unrepaired fault could not possibly remain in a living organism, since it can destroy the integrity of tissue structure and cause rapid failure of the organism. These traditional theories are all incomplete on interpreting aging phenomena. Nevertheless, developmental theory and damage (fault)-accumulation theory are more useful, because they have recognized the importance of damage and development process in aging. Some physical theories are useful, because they point out the common characteristics of aging changes, including loss of complexity, consequence of increase of entropy, and failure of information-transmission. An advanced theory, which can include all of these useful ideas in traditional theories, is needed.

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arXiv2017

Aging as a process of accumulation of Misrepairs

We recently introduced Misrepair-accumulation theory as an interpretation on aging mechanism. For better understanding this theory, we discuss here in more details the new concept of Misrepair and the concept of accumulation of Misrepairs. I. Aging takes place uniquely on the systems that have a well-defined structure: an organization of its sub-structures. Aging of a non-living system is a result of accumulation of injuries (damage) of its structure. II. A generalized concept of Misrepair is important for reaching to a unified understanding of aging changes. In the situation of a severe injury, incorrect repair is a repair essential for maintaining structural integrity for increasing the surviving chance of an organism. With the same mechanism as that in "Misrepair of DNA" , the term of "Misrepair" can be used for describing all kinds of incorrect repairs on different types of living structures, including molecules, cells and tissues. A new concept of Misrepair is therefore proposed and defined as incorrect reconstruction of an injured living structure. Misrepair mechanism is beneficial for the survival of an organism, and it is essential for the survival of a species. III. Alteration of structure made by Misrepair is irreversible; therefore Misrepairs accumulate and disorganize gradually a structure, which appears as aging of it. Accumulation of Misrepairs takes place on molecular, cellular and tissue levels respectively: on tissue level, it appears as disorganization of cells and extracellular matrixes (ECMs); on cellular level, it appears as deformation of cytoskeleton and change of cell shape; and on DNA, it appears as accumulation of DNA mutations and alteration of DNA sequence. An essential change in aging of an organism is an irreversible change of the spatial relationship between cells/ECMs in a tissue. In conclusion, aging of an organism is a result of accumulation of Misrepairs on tissue level.

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