The effect of thyroid hormone on mitochondrial biogenesis and cellular hyperplasia

Wooten, Wendy L.; Cascarano, Joseph

doi:10.1007/bf00745009

Cited by 21 publications

(8 citation statements)

References 39 publications

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“…1994). Exogenous thyroid hormone T4 increases mitochondrial volume density increases in both liver and muscle in rats (Wooten & Cascarano 1980, Goldenthal et al. 2004).…”

Section: Hormones and Mitochondrial Biogenesismentioning

confidence: 99%

Regulation of skeletal muscle mitochondrial function: genes to proteins

Lanza¹,

Nair²

2010

Acta Physiologica

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The impact of aging on mitochondrial function and the deterministic role of mitochondria on scenescence continue to be topics of vigorous debate. Many studies report that skeletal muscle mitochondrial content and function are reduced with aging and metabolic diseases associated with insulin resistance. However, an accumulating body of literature suggests that physical inactivity typical of aging may be a more important determinant of mitochondrial function than chronological age, per se. Reports of age-related declines in mitochondrial function have spawned a vast body of literature devoted to understanding the underlying mechanisms. These mechanisms include decreased abundance of mtDNA, reduced mRNA levels, as well as decreased synthesis and expression of mitochondrial proteins, ultimately resulting in decreased function of the whole organelle. Effective therapies to prevent reverse, or delay the onset of the aformentioned mitochondrial changes, regardless of their inevitability or precise underlying causes, require an intimate understanding of the processes that regulate mitochondrial biogenesis, which necessitates the coordinated regulation of nuclear and mitochondrial genomes. Herein we review the current thinking on regulation of mitochondrial biogenesis by transcription factors and transcriptional co-activators and the role of hormones and exercise in initiating this process. We review how exercise may help preserve mitochondrial content and functionality across the lifespan, and how physical inactivity is emerging as a major determinant of many age-associated changes at the level of the mitochondrion. We also review evidence that some mitochondrial changes with aging are independent of exercise or physical activity and appear to be inevitable consequences of old age.

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“…1994). Exogenous thyroid hormone T4 increases mitochondrial volume density increases in both liver and muscle in rats (Wooten & Cascarano 1980, Goldenthal et al. 2004).…”

Section: Hormones and Mitochondrial Biogenesismentioning

confidence: 99%

Regulation of skeletal muscle mitochondrial function: genes to proteins

Lanza¹,

Nair²

2010

Acta Physiologica

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“…Treatment of rats with the thyroid hormone T4 produces hyperplasia and increases the number and mass of mitochondria in both liver (Wooten & Cascarano, 1980) and cardiac muscle (Goldenthal, Weiss & Marin-Garcia, 2004). Levels of T3 and T4 hormones have been regarded as important factors in the maintenance of proper mitochondriogenic rates during aging (Mutvei, et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial biogenesis and healthy aging

López-Lluch

Irusta

Navas

et al. 2008

Experimental Gerontology

317

220

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Aging is associated with an overall loss of function at the level of the whole organism that has origins in cellular deterioration. Most cellular components, including mitochondria, require continuous recycling and regeneration throughout the lifespan. Mitochondria are particularly susceptive to damage over time as they are the major bioenergetic machinery and source of oxidative stress in cells. Effective control of mitochondrial biogenesis and turnover, therefore, becomes critical for the maintenance of energy production, the prevention of endogenous oxidative stress and the promotion of healthy aging. Multiple endogenous and exogenous factors regulate mitochondrial biogenesis through the peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α). Activators of PGC-1α include nitric oxide, CREB and AMPK. Calorie restriction (CR) and resveratrol, a proposed CR mimetic, also increase mitochondrial biogenesis through activation of PGC-1α. Moderate exercise also mimics CR by inducing mitochondrial biogenesis. Negative regulators of PGC-1α such as RIP140 and 160MBP suppress mitochondrial biogenesis. Another mechanism involved in mitochondrial maintenance is mitochondrial fission/fusion and this process also involves an increasing number of regulatory proteins. Dysfunction of either biogenesis or fission/fusion of mitochondria is associated with diseases of the neuromuscular system and aging, and a greater understanding of the regulation of these processes should help us to ultimately control the aging process.

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“…An increase in the levels of the thyroid hormone thyroxine causes hyperplasia and increases the number and mass of mitochondria in liver and cardiac muscle (88,259). Steroid hormones also affect mitochondrial biogenesis in adipose tissue by either inhibiting (testosterone) or promoting (progesterone) the expression of transcription factors involved in this process (193).…”

Section: Mitochondrial Biogenesismentioning

confidence: 99%

Mitochondrial Turnover and Aging of Long-Lived Postmitotic Cells: The Mitochondrial–Lysosomal Axis Theory of Aging

Terman

Kurz

Navrátil

et al. 2010

Antioxidants & Redox Signaling

425

375

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It is now generally accepted that aging and eventual death of multicellular organisms is to a large extent related to macromolecular damage by mitochondrially produced reactive oxygen species, mostly affecting long-lived postmitotic cells, such as neurons and cardiac myocytes. These cells are rarely or not at all replaced during life and can be as old as the whole organism. The inherent inability of autophagy and other cellular-degradation mechanisms to remove damaged structures completely results in the progressive accumulation of garbage, including cytosolic protein aggregates, defective mitochondria, and lipofuscin, an intralysosomal indigestible material. In this review, we stress the importance of crosstalk between mitochondria and lysosomes in aging. The slow accumulation of lipofuscin within lysosomes seems to depress autophagy, resulting in reduced turnover of effective mitochondria. The latter not only are functionally deficient but also produce increased amounts of reactive oxygen species, prompting lipofuscinogenesis. Moreover, defective and enlarged mitochondria are poorly autophagocytosed and constitute a growing population of badly functioning organelles that do not fuse and exchange their contents with normal mitochondria. The progress of these changes seems to result in enhanced oxidative stress, decreased ATP production, and collapse of the cellular catabolic machinery, which eventually is incompatible with survival. Antioxid. Redox Signal. 12, 503-535.

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The effect of thyroid hormone on mitochondrial biogenesis and cellular hyperplasia

Cited by 21 publications

References 39 publications

Regulation of skeletal muscle mitochondrial function: genes to proteins

Regulation of skeletal muscle mitochondrial function: genes to proteins

Mitochondrial biogenesis and healthy aging

Mitochondrial Turnover and Aging of Long-Lived Postmitotic Cells: The Mitochondrial–Lysosomal Axis Theory of Aging

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