Ramanathan Lab
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Research

Four areas spanning muscle regeneration and aging, human tissue models, space biology, and cellular resilience.

We study how metabolic state governs whether human tissues repair, adapt or decline. These four areas share experimental systems and measurement platforms, but each begins with a distinct biological problem.

Differentiated human myoblasts stained for myosin heavy chain, with aligned myotubes in red and nuclei in blue

Muscle regeneration, aging and senescence

How metabolic state and lipid signalling shape muscle stem-cell decisions, tissue repair and loss of function with age.

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A whole bioengineered human muscle construct imaged with TMRM, showing mitochondrial membrane potential across the tissue

Human tissue models

Bioengineered human muscle and motor neuron–muscle co-cultures for functional studies of aging, sarcopenia and treatment response.

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Loading human muscle stem cells into flight hardware before the Axiom-4 mission to the International Space Station

Space and microgravity biology

Human muscle stem cells in orbit, paired with ground-based simulation to investigate rapid deconditioning and recovery.

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Graphical abstract summarising the cellular effects of mild hypothermia and RBM3 on RNA, lipid metabolism, mitochondria and muscle differentiation

Cold and cellular resilience

How mild hypothermia and the cold-shock protein RBM3 reshape metabolism and help cells withstand environmental stress.

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Shared platforms, different questions

Bioengineered 3D organoids, Gravisim, metabolomics, Raman imaging and quantitative image analysis run through all four areas without flattening them into one programme.

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Skin: the same questions in a second tissue

Skin and skeletal muscle are not obvious neighbours, but they decline in similar ways. Both renew continuously from resident stem-cell pools, both lose that capacity as mitochondrial function falls and senescent cells accumulate, and both meet the environment directly. A mechanism worked out in muscle is therefore testable in skin — and one that holds in both tissues is more likely to be general than one demonstrated in either alone.

Our first step in that direction comes out of the cold work: whether the protective programmes engaged by mild hypothermia, RBM3 among them, can be induced in skin without sustained cooling. This is one line of work rather than a separate programme, and deliberately so. It begins with a mechanism we already understand, and asks how far it travels.

Skin research →

Where these areas lead

From mechanism to intervention

Each of the four areas above begins with a question about how muscle maintains or rebuilds itself. Several of them end somewhere more practical. The mechanisms we identify — metabolic, lipid-signalling, cold-responsive — become starting points for intervention, tested in the same bioengineered human tissue we use to study the biology and read against cohort measurements that show which changes matter in people.

This is not a fifth research area. It is the direction the others point, which is why the work sits inside them rather than beside them.

Several of these interventions are the subject of intellectual-property protection and are described here only in general terms.

Sarcopenia and precision medicine → Lipid signalling as a therapeutic target →

Ramanathan Lab · inStem, GKVK Campus, Bellary Road, Bangalore 560065, India arvind@instem.res.in

Last updated September 2026

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