Remodeling of Mitochondria in Cancer and Other Diseases

Article Biochemistry & Molecular Biology

Platelet Mitochondrial Bioenergetics Reprogramming in Patients with Urothelial Carcinoma

Patrik Palacka et al.

Summary: This study found that patients with urothelial carcinoma (UC) have deficient platelet mitochondrial function, decreased antioxidant levels, and increased oxidative stress. These changes are consistent with cell metabolism reprogramming in UC patients.

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES (2022)

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Article Oncology

ATAD3A mediates activation of RAS-independent mitochondrial ERK1/2 signaling, favoring head and neck cancer development

Liwei Lang et al.

Summary: Targeting mitochondrial oncoproteins presents a new concept for effective cancer therapeutics. In this study, the researchers focused on ATAD3A and its impact on head and neck squamous cell carcinoma (HNSCC). They found that ATAD3A is highly expressed in HNSCC tissues and cell lines, and loss of ATAD3A expression suppresses HNSCC cell growth and leads to tumor regression. Mechanistically, they discovered that ATAD3A interacts with ERK1/2 in the mitochondria of HNSCC cells and this interaction is essential for the activation of mitochondrial ERK1/2 signaling. Most importantly, they showed that targeting ATAD3A in combination with RAS inhibitor treatment has a more significant tumor suppression effect. These findings highlight the potential of ATAD3A and RAS signaling as targets for HNSCC therapeutics.

JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH (2022)

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Review Medicine, Research & Experimental

Mitochondrial dysfunction in cell senescence and aging

Satomi Miwa et al.

Summary: This article summarizes the importance of mitochondrial dysfunction in aging and cell senescence, discusses its relationship with cellular senescence, and proposes an anti-aging therapy that targets mitochondrial dysfunction.

JOURNAL OF CLINICAL INVESTIGATION (2022)

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Article Biochemistry & Molecular Biology

Mitochondrial Transfer Improves Cardiomyocyte Bioenergetics and Viability in Male Rats Exposed to Pregestational Diabetes

Eli J. Louwagie et al.

Summary: Offspring born to diabetic or obese mothers have a higher lifetime risk of heart disease. Research has shown that exposure to late-gestational diabetes mellitus (LGDM) or maternal high-fat (HF) diet can lead to mitochondrial dysfunction, impaired cardiomyocyte bioenergetics, and cardiac dysfunction in rat offspring. Findings suggest that mitochondrial dysfunction may play a central role in neonatal cardiomyopathy, with sex-specific differences observed in mitochondria-mediated mechanisms of heart disease development. Therapeutic mitochondrial transfer may have potential limitations, such as inconsistent effects in male and female offspring.