Your topics. New publications.

A compact browser notification when there’s something new. At most once a day — no account needed.

What interests you?

Optional and switchable off here at any time. We save your selected topics and device subscription; no email address is required. Privacy

Search the harborEN/DEAccount
Hallmarks of aging
Research brief

Review: metabolic kinases and inter-organelle communication in aging

This review links kinases such as AMPK, PDKs, mTOR, AKT and PERK to coordination between organelles in aging and age-related diseases, but notes that many effects on inter-organelle communication are indirect or inferred. [1]

Automatic summary · not editorially reviewed

The key findings

  1. The review states that mechanisms linking kinase signaling to specific inter-organelle contact sites or communication pathways remain incompletely defined. [1]

  2. The kinases discussed include AMPK, pyruvate dehydrogenase kinases, mTOR, AKT and PERK. [1]

  3. In many cases the effects on inter-organelle communication are indirect or inferred from broader changes in organelle function. [1]

The source at a glance

Study type / format
Review (abstract only)
Population / context
Cellular aging and age-related diseases, as discussed in a review of kinase signaling and organelle communication.
Summary based on
Study abstract
Original publication
July 1, 2026

Kinases and organelle coordination in aging

The review starts from the idea that cellular aging brings progressive changes in metabolic balance, stress adaptation and organelle function. It asks how signaling by metabolic and stress-responsive kinases relates to communication among membrane-bound organelles, including mitochondria, the endoplasmic reticulum, lysosomes, peroxisomes and the Golgi apparatus. The authors state that the mechanisms linking kinase signaling to specific contact sites or communication pathways remain incompletely defined.

Supporting source [1]

What the kinases are reported to regulate

The kinases discussed are AMPK, pyruvate dehydrogenase kinases (PDKs), mTOR, AKT and PERK. According to the review, they regulate mitochondrial dynamics, metabolic flux, calcium and lipid handling, autophagy, lysosomal function, proteostasis and vesicular trafficking. In some contexts kinase signaling meets defined organelle interfaces such as mitochondria-associated ER membranes; in many cases, however, effects on inter-organelle communication are indirect or inferred from broader changes in organelle function.

Supporting source [1]

Disease contexts and the review's stated limits

The review discusses how kinase dysregulation may contribute to age-associated defects in mitochondria-ER, mitochondria-lysosome, mitochondria-peroxisome and ER-Golgi coordination in neurodegeneration, cardiometabolic disease, cellular senescence and inflammaging. It presents kinase-regulated organelle communication as an emerging but still incompletely resolved framework for understanding cellular decline during aging. The abstract does not report a study design, sample or measured outcomes; it describes a review, and the full text was not reviewed.

Supporting source [1]

How to interpret this

Abstract only; the full text was not reviewed. The abstract describes a review and reports no study design, sample, follow-up or measured outcomes. It presents an emerging framework and notes that many links between kinases and inter-organelle communication are indirect or inferred.

Based on the study abstract; the full paper, tables and supplementary data were not reviewed.

Source & supporting passages

[1]
Read the quoted passagesIn the language of the original source
  1. Finding 1 ↑

    remain incompletely defined
  2. Finding 2 ↑

    including AMPK, pyruvate dehydrogenase kinases (PDKs), mTOR,
  3. Finding 3 ↑

    indirect or inferred from broader changes in

AI-assisted summary with linked source passages. No independent editorial or clinical review.

Our editorial method

Discussion

Community discussions

0 topics

Member contributions. Share sources, disclose commercial interests, and avoid personal medical or dosing advice.

Loading…