The role of mitochondria in aging of skeletal muscle

• Type: Another Publication in an International Scientific Journal
• Date: 2008

Authors

figueiredo, pa (Author) Other; mota, mp (Author) Other; appell, hj (Author) Other; duarte, ja (Author) FADEUP

Journal

Title: Biogerontology

Vol. 9

Pages: 67-84

ISSN: 1389-5729

Publisher: Springer Nature

Indexing

ISI Web of Knowledge - 61 Citations

Scopus - 76 Citations

Scientific classification

FOS: Medical and Health sciences > Clinical medicine

Other information

Authenticus ID: P-004-09N

DOI: 10.1007/s10522-007-9121-7

Abstract (EN): Aging can be characterized as a time dependent decline of maximal functionality that affects tissues and organs of the whole body. Such is induced by the progressive loss of redundant components and leads to an increased susceptibility to disease and risk of death. Regarding the aging of skeletal muscle, it has been pointed out that mitochondria is a key factor behind the loss of redundancy and functionality, since this organelle has a major role in cellular homeostasis particularly at the level of the bioenergetic status. Decreased activities of the mitochondrial electron transport chain complexes and an increased release of reactive oxygen species from mitochondria are well documented with age; it is suggested that the mitochondrial loss of function results from the increased oxidative damage to proteins, lipids, and DNA of this organelle. However, it is important to be aware that the mitochondrial loss of function could also be a consequence, rather than a cause, of the cellular deterioration with age, which compromises mitochondrial biogenesis, mitochondrial protein turnover and autophagocytosis of damaged mitochondria. In this review several topics will be addressed regarding the age-related loss of skeletal muscle redundancy associated with mitochondrial dysfunction, emphasizing hypotheses for underlying mechanisms. In addition, we discuss some of the cellular mechanisms that can be pointed out as being responsible for the age-related mitochondrial dysfunction.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 18