Publications by authors named "Gayathri K Natarajan"
Ample data support a prominent role of peripheral T-type calcium channels 3.2 (Ca V 3.2) in generating pain states.
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- Nearly 20 years after being identified as a gene linked to Wolf-Hirschhorn Syndrome, the exact role of the LETM1 protein in the inner mitochondrial membrane remains unclear.
- LETM1 is believed to influence key cellular functions like development, respiration, metabolism, and programmed cell death (apoptosis).
- This mini-review discusses the various cellular functions affected by LETM1 and emphasizes its importance in both health and disease contexts.
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- Mitochondrial calcium (Ca) handling is regulated through a balance of Ca uptake via the mitochondrial calcium uniporter (MCU), Ca buffering, and efflux via exchangers like Na/Ca (NCLX) and Ca/H (CHE) exchangers.
- This study examined Ca efflux through CHE in rat cardiac mitochondria, finding that factors like the amount of matrix Ca and external pH significantly influence this process, with acidic pH enhancing Ca efflux and ADP reducing it.
- Results suggest that the CHE's role in cardiac mitochondria is more complex than previously thought, potentially involving interactions with matrix Ca levels and pH changes, along with a potential contribution from LETM1
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- Mitochondrial free Ca regulation is essential for maintaining cellular balance, and increased levels can trigger the opening of the permeability transition pore (mPTP).
- Cyclosporin A (CsA) can delay this pore opening by inhibiting cyclophilin D and enhancing the sequestration of matrix free Ca, which helps stabilize calcium levels.
- In experiments with cardiac mitochondria, CsA improved the retention of baseline Ca levels, supporting normal mitochondrial functions like NADH levels and membrane potential, but this effect was lost without inorganic phosphate (P), highlighting the importance of P in maintaining mitochondrial Ca buffering and overall function.