Muscle Fiber and Satellite Cell Apoptosis in the Aging Human Thyroarytenoid Muscle: A Stereological Study with Confocal Laser Scanning Microscopy

Malmgren, Leslie T.; Jones, Christine E.; Bookman, Linda M.

doi:10.1067/mhn.2001.116449

Cited by 36 publications

(25 citation statements)

References 21 publications

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“…Despite the fact that most studies in animal models appear to support a key role for apoptosis in age-related muscle atrophy, evidence in humans is still scarce. As a result, to date only three reports have been published examining the occurrence and severity of myocyte apoptosis in healthy elderly humans (Malmgren et al, 2001; Park et al, 2009b; Whitman et al, 2005). In fact, a recent report indicated increases in the expression of the mitochondrial caspase-independent mediator apoptosis inducing factor (AIF) in semitendinosus muscle of middle-aged men relative to younger controls (Park et al, 2009b).…”

Section: Potential Mechanistic Triggers Of Sarcopeniamentioning

confidence: 99%

Models of accelerated sarcopenia: Critical pieces for solving the puzzle of age-related muscle atrophy

Buford¹,

Anton²,

Judge³

et al. 2010

Ageing Research Reviews

257

180

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Sarcopenia, the age-related loss of skeletal muscle mass, is a significant public health concern that continues to grow in relevance as the population ages. Certain conditions have the strong potential to coincide with sarcopenia to accelerate the progression of muscle atrophy in older adults. Among these conditions are co-morbid diseases common to older individuals such as cancer, kidney disease, diabetes, and peripheral artery disease. Furthermore, behaviors such as poor nutrition and physical inactivity are well-known to contribute to sarcopenia development. However, we argue that these behaviors are not inherent to the development of sarcopenia but rather accelerate its progression. In the present review, we discuss how these factors affect systemic and cellular mechanisms that contribute to skeletal muscle atrophy. In addition, we describe gaps in the literature concerning the role of these factors in accelerating sarcopenia progression. Elucidating biochemical pathways related to accelerated muscle atrophy may allow for improved discovery of therapeutic treatments related to sarcopenia.

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Section: Potential Mechanistic Triggers Of Sarcopeniamentioning

confidence: 99%

Models of accelerated sarcopenia: Critical pieces for solving the puzzle of age-related muscle atrophy

Buford¹,

Anton²,

Judge³

et al. 2010

Ageing Research Reviews

257

180

View full text Add to dashboard Cite

show abstract

“…To date, only three reports have been published examining the occurrence of myocyte apoptosis in older persons [11,16,83]. However, none of these studies has examined either specific biochemical pathways of apoptosis or functional implications.…”

Section: The Involvement Of Myocyte Apoptosis In Human Sarcopeniamentioning

confidence: 99%

Multiple Pathways to the Same End: Mechanisms of Myonuclear Apoptosis in Sarcopenia of Aging

Marzetti

Privitera

Simili

et al. 2010

The Scientific World JOURNAL

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Sarcopenia, the age-related decline in muscle mass and function, represents a significant health issue due to the high prevalence of frailty and disability associated with this condition. Nevertheless, the cellular mechanisms responsible for the loss of muscle mass in old age are still largely unknown. An altered regulation of myocyte apoptosis has recently emerged as a possible contributor to the pathogenesis of sarcopenia. Studies in animal models have shown that the severity of skeletal muscle apoptosis increases over the course of aging and correlates with the degree of muscle mass and strength decline. Several apoptotic pathways are operative in aged muscles, with the mitochondria- and TNF-α-mediated pathways likely being the most relevant to sarcopenia. However, despite the growing number of studies on the subject, a definite mechanistic link between myocyte apoptosis and age-related muscle atrophy has not yet been established. Furthermore, the evidence on the role played by apoptosis in human sarcopenia is still sparse. Clearly, further research is required to better define the involvement of myocyte apoptosis in the pathogenesis of muscle loss at advanced age. This knowledge will likely help in the design of more effective therapeutic strategies to preserve muscle mass into old age, thus fostering independence of the elderly population and reducing the socioeconomic burden associated with sarcopenia.

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“…(2011). In human muscle, increased levels of TUNEL‐positive nuclei have been detected from biopsies (Strasser et al ., 1999; Malmgren et al ., 2001; Whitman et al ., 2005). An increase in caspase‐3 levels was not detected (Whitman et al ., 2005).…”

Section: Introductionmentioning

confidence: 99%

Apoptosis and necrosis mediate skeletal muscle fiber loss in age‐induced mitochondrial enzymatic abnormalities

et al. 2015

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SummarySarcopenia, the age‐induced loss of skeletal muscle mass and function, results from the contributions of both fiber atrophy and loss of myofibers. We have previously characterized sarcopenia in FBN rats, documenting age‐dependent declines in muscle mass and fiber number along with increased fiber atrophy and fibrosis in vastus lateralis and rectus femoris muscles. Concomitant with these sarcopenic changes is an increased abundance of mitochondrial DNA deletion mutations and electron transport chain (ETC) abnormalities. In this study, we used immunohistological and histochemical approaches to define cell death pathways involved in sarcopenia. Activation of muscle cell death pathways was age‐dependent with most apoptotic and necrotic muscle fibers exhibiting ETC abnormalities. Although activation of apoptosis was a prominent feature of electron transport abnormal muscle fibers, necrosis was predominant in atrophic and broken ETC‐abnormal fibers. These data suggest that mitochondrial dysfunction is a major contributor to the activation of cell death processes in aged muscle fibers. The link between ETC abnormalities, apoptosis, fiber atrophy, and necrosis supports the hypothesis that mitochondrial DNA deletion mutations are causal in myofiber loss. These studies suggest a progression of events beginning with the generation and accumulation of a mtDNA deletion mutation, the concomitant development of ETC abnormalities, a subsequent triggering of apoptotic and, ultimately, necrotic events resulting in muscle fiber atrophy, breakage, and fiber loss.

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Muscle Fiber and Satellite Cell Apoptosis in the Aging Human Thyroarytenoid Muscle: A Stereological Study with Confocal Laser Scanning Microscopy

Abstract: Therapeutic techniques based on decreasing the frequency of apoptosis may block age-related fiber loss and atrophy in the TA.

Cited by 36 publications

References 21 publications

Models of accelerated sarcopenia: Critical pieces for solving the puzzle of age-related muscle atrophy

Models of accelerated sarcopenia: Critical pieces for solving the puzzle of age-related muscle atrophy

Multiple Pathways to the Same End: Mechanisms of Myonuclear Apoptosis in Sarcopenia of Aging

Apoptosis and necrosis mediate skeletal muscle fiber loss in age‐induced mitochondrial enzymatic abnormalities

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